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murine pca cell line rm  (ATCC)


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    ATCC murine pca cell line rm
    ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated <t>with</t> <t>RM-1</t> cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).
    Murine Pca Cell Line Rm, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 229 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/murine pca cell line rm/product/ATCC
    Average 96 stars, based on 229 article reviews
    murine pca cell line rm - by Bioz Stars, 2026-05
    96/100 stars

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    1) Product Images from "PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer"

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI197157

    ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated with RM-1 cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).
    Figure Legend Snippet: ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated with RM-1 cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).

    Techniques Used: Expressing, Whisker Assay, Immunohistochemical staining, Staining, Immunofluorescence, Flow Cytometry, Comparison

    ( A ) Paired peripheral blood serum samples from 5 PCa patients before and after PARPi treatment were analyzed using proteomics profiling. ( B ) Heatmap showing changes in serum protein profiles before and after PARPi treatment. ( C and D ) RT-qPCR analysis of PARPi-induced changes in CypA mRNA levels in murine PCa cell lines ( C ) and human PCa cell lines ( D ); N = 3 per group. ( E and F ) Western blot analysis of PARPi-induced changes in intracellular CypA (cCypA) and eCypA protein levels in murine ( E ) and human ( F ) PCa cell lines. ( G and H ) ELISA of PARPi-induced changes in CypA supernatant levels in murine ( G ) and human ( H ) PCa cell lines. ( I and J ) DCFH-DA (green) staining to detect PARPi-induced ROS levels in PCa cell lines RM-1 ( I ; N = 3) and MycCap/DU145/22RV1 ( J ; N = 5). Original magnification, ×100. ( K ) Gene Ontology enrichment analysis showing enhanced intracellular transport pathways in PCa cells after PARPi stimulation. ( L ) Western blot analysis of cCypA and eCypA levels after protein transport inhibition by Brefeldin A (BFA). Data are presented as mean ± SEM and were analyzed by Welch’s t test.
    Figure Legend Snippet: ( A ) Paired peripheral blood serum samples from 5 PCa patients before and after PARPi treatment were analyzed using proteomics profiling. ( B ) Heatmap showing changes in serum protein profiles before and after PARPi treatment. ( C and D ) RT-qPCR analysis of PARPi-induced changes in CypA mRNA levels in murine PCa cell lines ( C ) and human PCa cell lines ( D ); N = 3 per group. ( E and F ) Western blot analysis of PARPi-induced changes in intracellular CypA (cCypA) and eCypA protein levels in murine ( E ) and human ( F ) PCa cell lines. ( G and H ) ELISA of PARPi-induced changes in CypA supernatant levels in murine ( G ) and human ( H ) PCa cell lines. ( I and J ) DCFH-DA (green) staining to detect PARPi-induced ROS levels in PCa cell lines RM-1 ( I ; N = 3) and MycCap/DU145/22RV1 ( J ; N = 5). Original magnification, ×100. ( K ) Gene Ontology enrichment analysis showing enhanced intracellular transport pathways in PCa cells after PARPi stimulation. ( L ) Western blot analysis of cCypA and eCypA levels after protein transport inhibition by Brefeldin A (BFA). Data are presented as mean ± SEM and were analyzed by Welch’s t test.

    Techniques Used: Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Inhibition

    ( A ) Immunohistochemical staining of CypA in tumor tissues from patients with high- and low-grade PCa, collected at Tongji Hospital. Scale bars: 100 μm. ( B ) Proportional statistics of NCR1 expression in patients with high-grade versus intermediate/low-grade PCa; N = 5 per group. ( C ) Tumor growth curves and weights in C57BL/6 mice inoculated with RM-1 (vehicle/CypA-OE) cell lines; N = 5 per group. Scale bars: 1 cm. ( D ) Flow cytometry analysis of NK cell proportions in tumors of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( E and F ) Flow cytometry analysis of GZMB + ( E ; N = 5) and CXCR1 + ( F ; N = 6) proportions in TINKs from mice bearing CypA-OE RM-1 cells. ( G ) Flow cytometry analysis of NK cell proportions in peripheral blood of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( H and I ) Flow cytometry analysis of IFN-γ + ( H ) and TNF + ( I ) proportions in PBNKs from mice bearing CypA-OE RM-1 cells; N = 5 per group. ( J ) Tumor growth curves and weights in immunodeficient mice bearing CypA-OE tumors; N = 5 per group. Scale bars: 1 cm. ( K ) Tumor growth curves and weights in NK cell–depleted C57BL/6 mice inoculated with CypA-OE RM-1 cell lines; N = 5 per group; Scale bars: 1 cm. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( K ) and Welch’s t test ( C – J ).
    Figure Legend Snippet: ( A ) Immunohistochemical staining of CypA in tumor tissues from patients with high- and low-grade PCa, collected at Tongji Hospital. Scale bars: 100 μm. ( B ) Proportional statistics of NCR1 expression in patients with high-grade versus intermediate/low-grade PCa; N = 5 per group. ( C ) Tumor growth curves and weights in C57BL/6 mice inoculated with RM-1 (vehicle/CypA-OE) cell lines; N = 5 per group. Scale bars: 1 cm. ( D ) Flow cytometry analysis of NK cell proportions in tumors of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( E and F ) Flow cytometry analysis of GZMB + ( E ; N = 5) and CXCR1 + ( F ; N = 6) proportions in TINKs from mice bearing CypA-OE RM-1 cells. ( G ) Flow cytometry analysis of NK cell proportions in peripheral blood of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( H and I ) Flow cytometry analysis of IFN-γ + ( H ) and TNF + ( I ) proportions in PBNKs from mice bearing CypA-OE RM-1 cells; N = 5 per group. ( J ) Tumor growth curves and weights in immunodeficient mice bearing CypA-OE tumors; N = 5 per group. Scale bars: 1 cm. ( K ) Tumor growth curves and weights in NK cell–depleted C57BL/6 mice inoculated with CypA-OE RM-1 cell lines; N = 5 per group; Scale bars: 1 cm. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( K ) and Welch’s t test ( C – J ).

    Techniques Used: Immunohistochemical staining, Staining, Expressing, Flow Cytometry, Comparison

    ( A ) Apoptosis levels of RM-1 cells (transfected with CypA plasmid or vehicle control) cocultured with mouse NK cells at ratios of 1:0, 1:5, and 1:10 for 24 hours, as assessed by annexin V/PI staining. ( B ) Experimental design of the tumor cell–NK cell coculture killing assay. Original magnification, ×100. ( C ) Coculture system of tdTomato-labeled (red) RM-1–vehicle control cells and BFP-labeled (blue) RM-1–CypA-OE cells at equal numbers. Apoptosis rates of fluorescently labeled tumor cells after 24 h NK cell–mediated killing, as determined by flow cytometry; N = 6 per group. BFP, blue fluorescent protein. ( D and E ) IFN-γ ( D ) and GZMB ( E ) levels in NK cells cocultured with RM-1 cells (as described in A ); N = 5. ( F ) Purified mouse splenic NK cells (purity validated) cultured with recombinant CypA protein or isotype control. ( G and H ) Flow cytometry analysis of TNF-α and IFN-γ levels ( G ) and statistical quantification ( H ) in NK cells treated with recombinant CypA or isotype control; N = 5. ( I ) RNA-seq analysis of transcriptomic changes in NK cells exposed to CypA. ( J ) KEGG enrichment analysis showing upregulated oxidative phosphorylation in NK cells. ( K – N ) Cellular energy metabolism analysis: oxygen consumption rate ( K and L ) and extracellular acidification rate ( M and N ) in NK cells. ( O and P ) Mitochondrial membrane potential assay evaluating aerobic respiration capacity ( O ) and statistical results ( P ) in NK cells; N = 4. Data are presented as mean ± SEM and were analyzed by Welch’s t test.
    Figure Legend Snippet: ( A ) Apoptosis levels of RM-1 cells (transfected with CypA plasmid or vehicle control) cocultured with mouse NK cells at ratios of 1:0, 1:5, and 1:10 for 24 hours, as assessed by annexin V/PI staining. ( B ) Experimental design of the tumor cell–NK cell coculture killing assay. Original magnification, ×100. ( C ) Coculture system of tdTomato-labeled (red) RM-1–vehicle control cells and BFP-labeled (blue) RM-1–CypA-OE cells at equal numbers. Apoptosis rates of fluorescently labeled tumor cells after 24 h NK cell–mediated killing, as determined by flow cytometry; N = 6 per group. BFP, blue fluorescent protein. ( D and E ) IFN-γ ( D ) and GZMB ( E ) levels in NK cells cocultured with RM-1 cells (as described in A ); N = 5. ( F ) Purified mouse splenic NK cells (purity validated) cultured with recombinant CypA protein or isotype control. ( G and H ) Flow cytometry analysis of TNF-α and IFN-γ levels ( G ) and statistical quantification ( H ) in NK cells treated with recombinant CypA or isotype control; N = 5. ( I ) RNA-seq analysis of transcriptomic changes in NK cells exposed to CypA. ( J ) KEGG enrichment analysis showing upregulated oxidative phosphorylation in NK cells. ( K – N ) Cellular energy metabolism analysis: oxygen consumption rate ( K and L ) and extracellular acidification rate ( M and N ) in NK cells. ( O and P ) Mitochondrial membrane potential assay evaluating aerobic respiration capacity ( O ) and statistical results ( P ) in NK cells; N = 4. Data are presented as mean ± SEM and were analyzed by Welch’s t test.

    Techniques Used: Transfection, Plasmid Preparation, Control, Staining, Labeling, Flow Cytometry, Purification, Cell Culture, Recombinant, RNA Sequencing, Phospho-proteomics, Membrane

    ( A ) Tumor tissues were collected 14 days after inoculation with RM-1 cells in mice. TILs and TINKs were isolated. TILs were cultured with recombinant proteins in vitro, and recombinant protein tags were detected via flow cytometry. TINKs were cultured with recombinant proteins in vitro, and binding proteins were identified by IP-MS. FC, flow cytometry. ( B ) Venn diagram showing proteins with IP-MS scores ≥ 100 in TINKs, PBNKs, and PCa cells. ( C ) Proportion of membrane proteins versus nonmembrane proteins among overlapping proteins from B . ( D ) Membrane protein profiles identified by IP-MS. ( E ) Co-IP demonstrating mutual binding between ANXA6 and CypA-His. IB, immunoblotting. ( F ) Protein docking prediction between ANXA6 and CypA proteins using AlphaFold3. ( G ) Western blot analysis of ANXA6 expression and phosphorylation levels in NK cells treated with CypA and/or CsA. ( H ) Co-IP analysis of ANXA6 and FPR1 interaction in CypA-treated NK cells. ( I ) Fpr1 fl/fl mice were crossed with the Ncr1-iCre transgenic mice to generate the NK cell–specific Fpr1 -KO mice, which are denoted as Ncr1-iCre + -Fpr1 fl/fl . ( J ) Tumor growth curves and tumor weights in Fpr1 fl/fl and Ncr1-iCre + -Fpr1 fl/fl (cKO) mice inoculated with RM-1 vehicle or CypA-OE cells, respectively; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Tumor weight data are presented as mean ± SEM and were analyzed by 1-way ANOVA.
    Figure Legend Snippet: ( A ) Tumor tissues were collected 14 days after inoculation with RM-1 cells in mice. TILs and TINKs were isolated. TILs were cultured with recombinant proteins in vitro, and recombinant protein tags were detected via flow cytometry. TINKs were cultured with recombinant proteins in vitro, and binding proteins were identified by IP-MS. FC, flow cytometry. ( B ) Venn diagram showing proteins with IP-MS scores ≥ 100 in TINKs, PBNKs, and PCa cells. ( C ) Proportion of membrane proteins versus nonmembrane proteins among overlapping proteins from B . ( D ) Membrane protein profiles identified by IP-MS. ( E ) Co-IP demonstrating mutual binding between ANXA6 and CypA-His. IB, immunoblotting. ( F ) Protein docking prediction between ANXA6 and CypA proteins using AlphaFold3. ( G ) Western blot analysis of ANXA6 expression and phosphorylation levels in NK cells treated with CypA and/or CsA. ( H ) Co-IP analysis of ANXA6 and FPR1 interaction in CypA-treated NK cells. ( I ) Fpr1 fl/fl mice were crossed with the Ncr1-iCre transgenic mice to generate the NK cell–specific Fpr1 -KO mice, which are denoted as Ncr1-iCre + -Fpr1 fl/fl . ( J ) Tumor growth curves and tumor weights in Fpr1 fl/fl and Ncr1-iCre + -Fpr1 fl/fl (cKO) mice inoculated with RM-1 vehicle or CypA-OE cells, respectively; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Tumor weight data are presented as mean ± SEM and were analyzed by 1-way ANOVA.

    Techniques Used: Isolation, Cell Culture, Recombinant, In Vitro, Flow Cytometry, Binding Assay, Protein-Protein interactions, Membrane, Co-Immunoprecipitation Assay, Western Blot, Expressing, Phospho-proteomics, Transgenic Assay, Comparison

    ( A ) Tumor growth curves and weights in PARPi-treated tumor-bearing mice coadministered with CypA inhibitor CsA and FPR1 inhibitors CsH and HCH6-1; N = 6 per group; scale bars: 1 cm ( B ) Tumor growth curves and weights in C57BL/6 mice bearing RM-1 tumors treated with FPR1 agonist fMIFL or inhibitor HCH6-1; N = 5 per group; scale bars: 1 cm ( C and D ) IFN-γ and GZMB expression levels in TINKs ( C ) and their quantification ( D ) under HCH6-1 or fMIFL treatment; N = 5 per group. ( E ) Western blot analysis of ERK- and AKT-related pathway activation in NK cells treated with CypA, CsA, CsH, or HCH6-1 in vitro. ( F and G ) Flow cytometry analysis of IFN-γ and GZMB expression ( F ) and quantification ( G ) in NK cells treated with FPR1 inhibitor CsH, AKT inhibitor MK-2206, or ERK inhibitor SCH772984; N = 5 per group. ( H ) Transmission electron microscopy images showing mitochondrial structure and crista alterations in NK cells stimulated with CypA. Scale bars: 1 μm. ( I ) Statistical analysis of mitochondrial number ( N = 10) and crista count ( N = 15) in NK cells. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( A , B , D , and G ) and Welch’s t test ( I ).
    Figure Legend Snippet: ( A ) Tumor growth curves and weights in PARPi-treated tumor-bearing mice coadministered with CypA inhibitor CsA and FPR1 inhibitors CsH and HCH6-1; N = 6 per group; scale bars: 1 cm ( B ) Tumor growth curves and weights in C57BL/6 mice bearing RM-1 tumors treated with FPR1 agonist fMIFL or inhibitor HCH6-1; N = 5 per group; scale bars: 1 cm ( C and D ) IFN-γ and GZMB expression levels in TINKs ( C ) and their quantification ( D ) under HCH6-1 or fMIFL treatment; N = 5 per group. ( E ) Western blot analysis of ERK- and AKT-related pathway activation in NK cells treated with CypA, CsA, CsH, or HCH6-1 in vitro. ( F and G ) Flow cytometry analysis of IFN-γ and GZMB expression ( F ) and quantification ( G ) in NK cells treated with FPR1 inhibitor CsH, AKT inhibitor MK-2206, or ERK inhibitor SCH772984; N = 5 per group. ( H ) Transmission electron microscopy images showing mitochondrial structure and crista alterations in NK cells stimulated with CypA. Scale bars: 1 μm. ( I ) Statistical analysis of mitochondrial number ( N = 10) and crista count ( N = 15) in NK cells. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( A , B , D , and G ) and Welch’s t test ( I ).

    Techniques Used: Expressing, Western Blot, Activation Assay, In Vitro, Flow Cytometry, Transmission Assay, Electron Microscopy, Comparison

    ( A ) Mice bearing RM-1 tumors were treated with mefuparib and adoptive transfer of 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for tumor collection. ( B and C ) Tumor growth curves ( B ) and weights ( C ) in mice treated with adoptive NK cell therapy, PARPi, or combination therapy; N = 6; scale bars: 1 cm. ( D ) Immunofluorescence of tumors from mice treated with adoptive NK cells, PARPi, or combination therapy, showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 50 μm. ( E and F ) Quantification of average NK1.1 + cells ( E ) and GZMB + NK1.1 + cells ( F ) per high-power field. Data are based on average counts from 5 random fields per sample; N = 5. ( G ) Mice bearing orthotopic PPSM tumors received mefuparib and 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for analysis or retained for survival observation. ( H ) In vivo small animal imaging of orthotopic prostate tumor growth on day 18. ( I ) Survival curves of orthotopic PCa mouse models. ( J ) Western blot confirming hPSMA expression in DU145 cells. ( K ) Design of CAR-NK cells targeting human PSMA. SP, signal peptide; TM, transmembrane. ( L ) Representative flow cytometry analysis showing the transduction efficiency of CAR-NK cells. ( M ) Establishment of the DU145-hPSMA in situ PCa implantation model. Subsequently, tumor-bearing mice were treated with mefuparib and 10 5 CAR-NK cells every 2 days from day 8. Mice were euthanized on day 24 for tumor collection. ( N ) Tumor weight in DU145-hPSMA–bearing mice treated with PARPi and/or CAR-NK cells; N = 6. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Survival curves were analyzed by a log-rank (Mantel-Cox) test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA.
    Figure Legend Snippet: ( A ) Mice bearing RM-1 tumors were treated with mefuparib and adoptive transfer of 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for tumor collection. ( B and C ) Tumor growth curves ( B ) and weights ( C ) in mice treated with adoptive NK cell therapy, PARPi, or combination therapy; N = 6; scale bars: 1 cm. ( D ) Immunofluorescence of tumors from mice treated with adoptive NK cells, PARPi, or combination therapy, showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 50 μm. ( E and F ) Quantification of average NK1.1 + cells ( E ) and GZMB + NK1.1 + cells ( F ) per high-power field. Data are based on average counts from 5 random fields per sample; N = 5. ( G ) Mice bearing orthotopic PPSM tumors received mefuparib and 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for analysis or retained for survival observation. ( H ) In vivo small animal imaging of orthotopic prostate tumor growth on day 18. ( I ) Survival curves of orthotopic PCa mouse models. ( J ) Western blot confirming hPSMA expression in DU145 cells. ( K ) Design of CAR-NK cells targeting human PSMA. SP, signal peptide; TM, transmembrane. ( L ) Representative flow cytometry analysis showing the transduction efficiency of CAR-NK cells. ( M ) Establishment of the DU145-hPSMA in situ PCa implantation model. Subsequently, tumor-bearing mice were treated with mefuparib and 10 5 CAR-NK cells every 2 days from day 8. Mice were euthanized on day 24 for tumor collection. ( N ) Tumor weight in DU145-hPSMA–bearing mice treated with PARPi and/or CAR-NK cells; N = 6. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Survival curves were analyzed by a log-rank (Mantel-Cox) test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA.

    Techniques Used: Adoptive Transfer Assay, Immunofluorescence, In Vivo, Imaging, Western Blot, Expressing, Flow Cytometry, Transduction, In Situ, Comparison



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    murine pca cell line rm  (ATCC)
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    ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated <t>with</t> <t>RM-1</t> cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).
    Murine Pca Cell Line Rm, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/murine pca cell line rm/product/ATCC
    Average 96 stars, based on 1 article reviews
    murine pca cell line rm - by Bioz Stars, 2026-05
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    murine pca cell line rm1  (ATCC)
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    ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated <t>with</t> <t>RM-1</t> cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).
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    https://www.bioz.com/result/murine pca cell line rm1/product/ATCC
    Average 96 stars, based on 1 article reviews
    murine pca cell line rm1 - by Bioz Stars, 2026-05
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    murine pca cell lines  (ATCC)
    96
    ATCC murine pca cell lines
    A Full circle translational research design to explore the immunoregulatory effects of WBM in <t>PCa</t> patients. The initial single‐arm Phase I clinical trial involving WBM tablet consumption (NCT00779168) in PCa patients identified circulating MDSCs as immune <t>cells</t> responsive to WBM treatment. Building upon these findings, the current study includes experiments on PCa <t>murine</t> models and analysis of PCa patients in a dual‐centre, two‐arm, open‐label, randomised Phase II trial (NCT04519879). This bidirectional translational research approach has supported the immunomodulatory role of WBM on MDSCs, thus strengthening the rationale for using WBM as a nutraceutical approach to slow the progression of prostate cancer.
    Murine Pca Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/murine pca cell lines/product/ATCC
    Average 96 stars, based on 1 article reviews
    murine pca cell lines - by Bioz Stars, 2026-05
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    panc02 crl 2553 murine pca cell line  (ATCC)
    95
    ATCC panc02 crl 2553 murine pca cell line
    A Full circle translational research design to explore the immunoregulatory effects of WBM in <t>PCa</t> patients. The initial single‐arm Phase I clinical trial involving WBM tablet consumption (NCT00779168) in PCa patients identified circulating MDSCs as immune <t>cells</t> responsive to WBM treatment. Building upon these findings, the current study includes experiments on PCa <t>murine</t> models and analysis of PCa patients in a dual‐centre, two‐arm, open‐label, randomised Phase II trial (NCT04519879). This bidirectional translational research approach has supported the immunomodulatory role of WBM on MDSCs, thus strengthening the rationale for using WBM as a nutraceutical approach to slow the progression of prostate cancer.
    Panc02 Crl 2553 Murine Pca Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    murine metastatic pca rm1 cell line  (ATCC)
    96
    ATCC murine metastatic pca rm1 cell line
    (A) Three-dimensional and longitudinal cross-sectional μCT images of the tibia from control and <t>RM1</t> cell administered mice post-IPA-3 treatment. Analysis of trabecular bone (indicated by arrows) demonstrates significant loss of trabecular bone in RM1-injected tibia which was blunted upon treatment with 5 mg/kg/day IPA-3 (n=10). (B-C) A plot showing significantly reduced bone volume percentage and bone marrow density of trabecular area with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days. (D-E) A plot showing the significantly reduced trabecular number with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days (n=10). The trabecular thickness did not change between groups indicating that cancer cells do not affect trabecular thickness in the trabecular section of tibia. Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups. BV=Bone Volume, TV=Tissue Volume, BMD=Bone Marrow Density.
    Murine Metastatic Pca Rm1 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/murine metastatic pca rm1 cell line/product/ATCC
    Average 96 stars, based on 1 article reviews
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    murine pca cell line tramp c1  (ATCC)
    96
    ATCC murine pca cell line tramp c1
    (A) Three-dimensional and longitudinal cross-sectional μCT images of the tibia from control and <t>RM1</t> cell administered mice post-IPA-3 treatment. Analysis of trabecular bone (indicated by arrows) demonstrates significant loss of trabecular bone in RM1-injected tibia which was blunted upon treatment with 5 mg/kg/day IPA-3 (n=10). (B-C) A plot showing significantly reduced bone volume percentage and bone marrow density of trabecular area with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days. (D-E) A plot showing the significantly reduced trabecular number with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days (n=10). The trabecular thickness did not change between groups indicating that cancer cells do not affect trabecular thickness in the trabecular section of tibia. Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups. BV=Bone Volume, TV=Tissue Volume, BMD=Bone Marrow Density.
    Murine Pca Cell Line Tramp C1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/murine pca cell line tramp c1/product/ATCC
    Average 96 stars, based on 1 article reviews
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    Image Search Results


    ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated with RM-1 cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Expression of CD16, CD56, NCR1, and KLRF1 in PCa versus normal tissues (TCGA). The box-and-whisker plots depict the minimum and maximum values (whiskers), the upper and lower quartiles, and the median. ( B ) Immunohistochemical staining of NCR1 in high- and low-grade PCa tissues collected at Tongji Hospital. Scale bars: 100 μm. ( C ) Proportion of NCR1 expression in patients with high-grade ( N = 10) versus intermediate/low-grade ( N = 10) PCa. ( D ) Treatment regimens for C57BL/6 mice bearing CRPC-PPSM starting on day 8 after inoculation: enzalutamide (10 mg/kg, oral, daily), anti–PD-1 (200 μg/kg, i.p., every 3 days), docetaxel (10 mg/kg, i.v., weekly), and mefuparib (40 mg/kg, oral, every 2 days). Mice were euthanized on day 25 after tumor inoculation. ( E ) Tumor growth curves and tumor weights in mice from D for each treatment; N = 5 per group. Scale bars: 1 cm. ( F ) Immunofluorescence of tumors from D showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 20 μm. ( G ) Tumor growth curves and weights of C57BL/6 mice inoculated with RM-1 cells and treated with or without PARPi; N = 6 per group. Scale bars: 1 cm. ( H ) Tumor growth curves and weights of Rag1 – / – γc – / – mice inoculated with RM-1 or RM-1 BRCA1 -KO cells and treated with or without PARPi; N = 5 per group. Scale bars: 1 cm.( I – L ) Flow cytometry analysis of NK cell proportions in tumors ( I ) and peripheral blood ( K ), GZMB + proportion in TINKs ( J ), and TNF-α + IFN-γ + proportions in PBNKs ( L ) of mice from G ; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM. Data were analyzed by 1-way ANOVA ( E and H ) and Welch’s t test ( G and I – L ).

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Expressing, Whisker Assay, Immunohistochemical staining, Staining, Immunofluorescence, Flow Cytometry, Comparison

    ( A ) Paired peripheral blood serum samples from 5 PCa patients before and after PARPi treatment were analyzed using proteomics profiling. ( B ) Heatmap showing changes in serum protein profiles before and after PARPi treatment. ( C and D ) RT-qPCR analysis of PARPi-induced changes in CypA mRNA levels in murine PCa cell lines ( C ) and human PCa cell lines ( D ); N = 3 per group. ( E and F ) Western blot analysis of PARPi-induced changes in intracellular CypA (cCypA) and eCypA protein levels in murine ( E ) and human ( F ) PCa cell lines. ( G and H ) ELISA of PARPi-induced changes in CypA supernatant levels in murine ( G ) and human ( H ) PCa cell lines. ( I and J ) DCFH-DA (green) staining to detect PARPi-induced ROS levels in PCa cell lines RM-1 ( I ; N = 3) and MycCap/DU145/22RV1 ( J ; N = 5). Original magnification, ×100. ( K ) Gene Ontology enrichment analysis showing enhanced intracellular transport pathways in PCa cells after PARPi stimulation. ( L ) Western blot analysis of cCypA and eCypA levels after protein transport inhibition by Brefeldin A (BFA). Data are presented as mean ± SEM and were analyzed by Welch’s t test.

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Paired peripheral blood serum samples from 5 PCa patients before and after PARPi treatment were analyzed using proteomics profiling. ( B ) Heatmap showing changes in serum protein profiles before and after PARPi treatment. ( C and D ) RT-qPCR analysis of PARPi-induced changes in CypA mRNA levels in murine PCa cell lines ( C ) and human PCa cell lines ( D ); N = 3 per group. ( E and F ) Western blot analysis of PARPi-induced changes in intracellular CypA (cCypA) and eCypA protein levels in murine ( E ) and human ( F ) PCa cell lines. ( G and H ) ELISA of PARPi-induced changes in CypA supernatant levels in murine ( G ) and human ( H ) PCa cell lines. ( I and J ) DCFH-DA (green) staining to detect PARPi-induced ROS levels in PCa cell lines RM-1 ( I ; N = 3) and MycCap/DU145/22RV1 ( J ; N = 5). Original magnification, ×100. ( K ) Gene Ontology enrichment analysis showing enhanced intracellular transport pathways in PCa cells after PARPi stimulation. ( L ) Western blot analysis of cCypA and eCypA levels after protein transport inhibition by Brefeldin A (BFA). Data are presented as mean ± SEM and were analyzed by Welch’s t test.

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Inhibition

    ( A ) Immunohistochemical staining of CypA in tumor tissues from patients with high- and low-grade PCa, collected at Tongji Hospital. Scale bars: 100 μm. ( B ) Proportional statistics of NCR1 expression in patients with high-grade versus intermediate/low-grade PCa; N = 5 per group. ( C ) Tumor growth curves and weights in C57BL/6 mice inoculated with RM-1 (vehicle/CypA-OE) cell lines; N = 5 per group. Scale bars: 1 cm. ( D ) Flow cytometry analysis of NK cell proportions in tumors of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( E and F ) Flow cytometry analysis of GZMB + ( E ; N = 5) and CXCR1 + ( F ; N = 6) proportions in TINKs from mice bearing CypA-OE RM-1 cells. ( G ) Flow cytometry analysis of NK cell proportions in peripheral blood of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( H and I ) Flow cytometry analysis of IFN-γ + ( H ) and TNF + ( I ) proportions in PBNKs from mice bearing CypA-OE RM-1 cells; N = 5 per group. ( J ) Tumor growth curves and weights in immunodeficient mice bearing CypA-OE tumors; N = 5 per group. Scale bars: 1 cm. ( K ) Tumor growth curves and weights in NK cell–depleted C57BL/6 mice inoculated with CypA-OE RM-1 cell lines; N = 5 per group; Scale bars: 1 cm. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( K ) and Welch’s t test ( C – J ).

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Immunohistochemical staining of CypA in tumor tissues from patients with high- and low-grade PCa, collected at Tongji Hospital. Scale bars: 100 μm. ( B ) Proportional statistics of NCR1 expression in patients with high-grade versus intermediate/low-grade PCa; N = 5 per group. ( C ) Tumor growth curves and weights in C57BL/6 mice inoculated with RM-1 (vehicle/CypA-OE) cell lines; N = 5 per group. Scale bars: 1 cm. ( D ) Flow cytometry analysis of NK cell proportions in tumors of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( E and F ) Flow cytometry analysis of GZMB + ( E ; N = 5) and CXCR1 + ( F ; N = 6) proportions in TINKs from mice bearing CypA-OE RM-1 cells. ( G ) Flow cytometry analysis of NK cell proportions in peripheral blood of mice bearing CypA-OE RM-1 cells; N = 5 per group. ( H and I ) Flow cytometry analysis of IFN-γ + ( H ) and TNF + ( I ) proportions in PBNKs from mice bearing CypA-OE RM-1 cells; N = 5 per group. ( J ) Tumor growth curves and weights in immunodeficient mice bearing CypA-OE tumors; N = 5 per group. Scale bars: 1 cm. ( K ) Tumor growth curves and weights in NK cell–depleted C57BL/6 mice inoculated with CypA-OE RM-1 cell lines; N = 5 per group; Scale bars: 1 cm. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( K ) and Welch’s t test ( C – J ).

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Immunohistochemical staining, Staining, Expressing, Flow Cytometry, Comparison

    ( A ) Apoptosis levels of RM-1 cells (transfected with CypA plasmid or vehicle control) cocultured with mouse NK cells at ratios of 1:0, 1:5, and 1:10 for 24 hours, as assessed by annexin V/PI staining. ( B ) Experimental design of the tumor cell–NK cell coculture killing assay. Original magnification, ×100. ( C ) Coculture system of tdTomato-labeled (red) RM-1–vehicle control cells and BFP-labeled (blue) RM-1–CypA-OE cells at equal numbers. Apoptosis rates of fluorescently labeled tumor cells after 24 h NK cell–mediated killing, as determined by flow cytometry; N = 6 per group. BFP, blue fluorescent protein. ( D and E ) IFN-γ ( D ) and GZMB ( E ) levels in NK cells cocultured with RM-1 cells (as described in A ); N = 5. ( F ) Purified mouse splenic NK cells (purity validated) cultured with recombinant CypA protein or isotype control. ( G and H ) Flow cytometry analysis of TNF-α and IFN-γ levels ( G ) and statistical quantification ( H ) in NK cells treated with recombinant CypA or isotype control; N = 5. ( I ) RNA-seq analysis of transcriptomic changes in NK cells exposed to CypA. ( J ) KEGG enrichment analysis showing upregulated oxidative phosphorylation in NK cells. ( K – N ) Cellular energy metabolism analysis: oxygen consumption rate ( K and L ) and extracellular acidification rate ( M and N ) in NK cells. ( O and P ) Mitochondrial membrane potential assay evaluating aerobic respiration capacity ( O ) and statistical results ( P ) in NK cells; N = 4. Data are presented as mean ± SEM and were analyzed by Welch’s t test.

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Apoptosis levels of RM-1 cells (transfected with CypA plasmid or vehicle control) cocultured with mouse NK cells at ratios of 1:0, 1:5, and 1:10 for 24 hours, as assessed by annexin V/PI staining. ( B ) Experimental design of the tumor cell–NK cell coculture killing assay. Original magnification, ×100. ( C ) Coculture system of tdTomato-labeled (red) RM-1–vehicle control cells and BFP-labeled (blue) RM-1–CypA-OE cells at equal numbers. Apoptosis rates of fluorescently labeled tumor cells after 24 h NK cell–mediated killing, as determined by flow cytometry; N = 6 per group. BFP, blue fluorescent protein. ( D and E ) IFN-γ ( D ) and GZMB ( E ) levels in NK cells cocultured with RM-1 cells (as described in A ); N = 5. ( F ) Purified mouse splenic NK cells (purity validated) cultured with recombinant CypA protein or isotype control. ( G and H ) Flow cytometry analysis of TNF-α and IFN-γ levels ( G ) and statistical quantification ( H ) in NK cells treated with recombinant CypA or isotype control; N = 5. ( I ) RNA-seq analysis of transcriptomic changes in NK cells exposed to CypA. ( J ) KEGG enrichment analysis showing upregulated oxidative phosphorylation in NK cells. ( K – N ) Cellular energy metabolism analysis: oxygen consumption rate ( K and L ) and extracellular acidification rate ( M and N ) in NK cells. ( O and P ) Mitochondrial membrane potential assay evaluating aerobic respiration capacity ( O ) and statistical results ( P ) in NK cells; N = 4. Data are presented as mean ± SEM and were analyzed by Welch’s t test.

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Transfection, Plasmid Preparation, Control, Staining, Labeling, Flow Cytometry, Purification, Cell Culture, Recombinant, RNA Sequencing, Phospho-proteomics, Membrane

    ( A ) Tumor tissues were collected 14 days after inoculation with RM-1 cells in mice. TILs and TINKs were isolated. TILs were cultured with recombinant proteins in vitro, and recombinant protein tags were detected via flow cytometry. TINKs were cultured with recombinant proteins in vitro, and binding proteins were identified by IP-MS. FC, flow cytometry. ( B ) Venn diagram showing proteins with IP-MS scores ≥ 100 in TINKs, PBNKs, and PCa cells. ( C ) Proportion of membrane proteins versus nonmembrane proteins among overlapping proteins from B . ( D ) Membrane protein profiles identified by IP-MS. ( E ) Co-IP demonstrating mutual binding between ANXA6 and CypA-His. IB, immunoblotting. ( F ) Protein docking prediction between ANXA6 and CypA proteins using AlphaFold3. ( G ) Western blot analysis of ANXA6 expression and phosphorylation levels in NK cells treated with CypA and/or CsA. ( H ) Co-IP analysis of ANXA6 and FPR1 interaction in CypA-treated NK cells. ( I ) Fpr1 fl/fl mice were crossed with the Ncr1-iCre transgenic mice to generate the NK cell–specific Fpr1 -KO mice, which are denoted as Ncr1-iCre + -Fpr1 fl/fl . ( J ) Tumor growth curves and tumor weights in Fpr1 fl/fl and Ncr1-iCre + -Fpr1 fl/fl (cKO) mice inoculated with RM-1 vehicle or CypA-OE cells, respectively; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Tumor weight data are presented as mean ± SEM and were analyzed by 1-way ANOVA.

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Tumor tissues were collected 14 days after inoculation with RM-1 cells in mice. TILs and TINKs were isolated. TILs were cultured with recombinant proteins in vitro, and recombinant protein tags were detected via flow cytometry. TINKs were cultured with recombinant proteins in vitro, and binding proteins were identified by IP-MS. FC, flow cytometry. ( B ) Venn diagram showing proteins with IP-MS scores ≥ 100 in TINKs, PBNKs, and PCa cells. ( C ) Proportion of membrane proteins versus nonmembrane proteins among overlapping proteins from B . ( D ) Membrane protein profiles identified by IP-MS. ( E ) Co-IP demonstrating mutual binding between ANXA6 and CypA-His. IB, immunoblotting. ( F ) Protein docking prediction between ANXA6 and CypA proteins using AlphaFold3. ( G ) Western blot analysis of ANXA6 expression and phosphorylation levels in NK cells treated with CypA and/or CsA. ( H ) Co-IP analysis of ANXA6 and FPR1 interaction in CypA-treated NK cells. ( I ) Fpr1 fl/fl mice were crossed with the Ncr1-iCre transgenic mice to generate the NK cell–specific Fpr1 -KO mice, which are denoted as Ncr1-iCre + -Fpr1 fl/fl . ( J ) Tumor growth curves and tumor weights in Fpr1 fl/fl and Ncr1-iCre + -Fpr1 fl/fl (cKO) mice inoculated with RM-1 vehicle or CypA-OE cells, respectively; N = 5 per group. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Tumor weight data are presented as mean ± SEM and were analyzed by 1-way ANOVA.

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Isolation, Cell Culture, Recombinant, In Vitro, Flow Cytometry, Binding Assay, Protein-Protein interactions, Membrane, Co-Immunoprecipitation Assay, Western Blot, Expressing, Phospho-proteomics, Transgenic Assay, Comparison

    ( A ) Tumor growth curves and weights in PARPi-treated tumor-bearing mice coadministered with CypA inhibitor CsA and FPR1 inhibitors CsH and HCH6-1; N = 6 per group; scale bars: 1 cm ( B ) Tumor growth curves and weights in C57BL/6 mice bearing RM-1 tumors treated with FPR1 agonist fMIFL or inhibitor HCH6-1; N = 5 per group; scale bars: 1 cm ( C and D ) IFN-γ and GZMB expression levels in TINKs ( C ) and their quantification ( D ) under HCH6-1 or fMIFL treatment; N = 5 per group. ( E ) Western blot analysis of ERK- and AKT-related pathway activation in NK cells treated with CypA, CsA, CsH, or HCH6-1 in vitro. ( F and G ) Flow cytometry analysis of IFN-γ and GZMB expression ( F ) and quantification ( G ) in NK cells treated with FPR1 inhibitor CsH, AKT inhibitor MK-2206, or ERK inhibitor SCH772984; N = 5 per group. ( H ) Transmission electron microscopy images showing mitochondrial structure and crista alterations in NK cells stimulated with CypA. Scale bars: 1 μm. ( I ) Statistical analysis of mitochondrial number ( N = 10) and crista count ( N = 15) in NK cells. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( A , B , D , and G ) and Welch’s t test ( I ).

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Tumor growth curves and weights in PARPi-treated tumor-bearing mice coadministered with CypA inhibitor CsA and FPR1 inhibitors CsH and HCH6-1; N = 6 per group; scale bars: 1 cm ( B ) Tumor growth curves and weights in C57BL/6 mice bearing RM-1 tumors treated with FPR1 agonist fMIFL or inhibitor HCH6-1; N = 5 per group; scale bars: 1 cm ( C and D ) IFN-γ and GZMB expression levels in TINKs ( C ) and their quantification ( D ) under HCH6-1 or fMIFL treatment; N = 5 per group. ( E ) Western blot analysis of ERK- and AKT-related pathway activation in NK cells treated with CypA, CsA, CsH, or HCH6-1 in vitro. ( F and G ) Flow cytometry analysis of IFN-γ and GZMB expression ( F ) and quantification ( G ) in NK cells treated with FPR1 inhibitor CsH, AKT inhibitor MK-2206, or ERK inhibitor SCH772984; N = 5 per group. ( H ) Transmission electron microscopy images showing mitochondrial structure and crista alterations in NK cells stimulated with CypA. Scale bars: 1 μm. ( I ) Statistical analysis of mitochondrial number ( N = 10) and crista count ( N = 15) in NK cells. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA ( A , B , D , and G ) and Welch’s t test ( I ).

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Expressing, Western Blot, Activation Assay, In Vitro, Flow Cytometry, Transmission Assay, Electron Microscopy, Comparison

    ( A ) Mice bearing RM-1 tumors were treated with mefuparib and adoptive transfer of 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for tumor collection. ( B and C ) Tumor growth curves ( B ) and weights ( C ) in mice treated with adoptive NK cell therapy, PARPi, or combination therapy; N = 6; scale bars: 1 cm. ( D ) Immunofluorescence of tumors from mice treated with adoptive NK cells, PARPi, or combination therapy, showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 50 μm. ( E and F ) Quantification of average NK1.1 + cells ( E ) and GZMB + NK1.1 + cells ( F ) per high-power field. Data are based on average counts from 5 random fields per sample; N = 5. ( G ) Mice bearing orthotopic PPSM tumors received mefuparib and 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for analysis or retained for survival observation. ( H ) In vivo small animal imaging of orthotopic prostate tumor growth on day 18. ( I ) Survival curves of orthotopic PCa mouse models. ( J ) Western blot confirming hPSMA expression in DU145 cells. ( K ) Design of CAR-NK cells targeting human PSMA. SP, signal peptide; TM, transmembrane. ( L ) Representative flow cytometry analysis showing the transduction efficiency of CAR-NK cells. ( M ) Establishment of the DU145-hPSMA in situ PCa implantation model. Subsequently, tumor-bearing mice were treated with mefuparib and 10 5 CAR-NK cells every 2 days from day 8. Mice were euthanized on day 24 for tumor collection. ( N ) Tumor weight in DU145-hPSMA–bearing mice treated with PARPi and/or CAR-NK cells; N = 6. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Survival curves were analyzed by a log-rank (Mantel-Cox) test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA.

    Journal: The Journal of Clinical Investigation

    Article Title: PARP inhibitors restore NK cell function via secretory crosstalk with tumor cells in prostate cancer

    doi: 10.1172/JCI197157

    Figure Lengend Snippet: ( A ) Mice bearing RM-1 tumors were treated with mefuparib and adoptive transfer of 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for tumor collection. ( B and C ) Tumor growth curves ( B ) and weights ( C ) in mice treated with adoptive NK cell therapy, PARPi, or combination therapy; N = 6; scale bars: 1 cm. ( D ) Immunofluorescence of tumors from mice treated with adoptive NK cells, PARPi, or combination therapy, showing DAPI (blue), NK1.1 (red), GZMB (yellow), and PanCK (white). Scale bars: 50 μm. ( E and F ) Quantification of average NK1.1 + cells ( E ) and GZMB + NK1.1 + cells ( F ) per high-power field. Data are based on average counts from 5 random fields per sample; N = 5. ( G ) Mice bearing orthotopic PPSM tumors received mefuparib and 10 5 NK cells every 2 days from day 8. Mice were euthanized on day 18 for analysis or retained for survival observation. ( H ) In vivo small animal imaging of orthotopic prostate tumor growth on day 18. ( I ) Survival curves of orthotopic PCa mouse models. ( J ) Western blot confirming hPSMA expression in DU145 cells. ( K ) Design of CAR-NK cells targeting human PSMA. SP, signal peptide; TM, transmembrane. ( L ) Representative flow cytometry analysis showing the transduction efficiency of CAR-NK cells. ( M ) Establishment of the DU145-hPSMA in situ PCa implantation model. Subsequently, tumor-bearing mice were treated with mefuparib and 10 5 CAR-NK cells every 2 days from day 8. Mice were euthanized on day 24 for tumor collection. ( N ) Tumor weight in DU145-hPSMA–bearing mice treated with PARPi and/or CAR-NK cells; N = 6. Tumor growth curve data are presented as mean ± SD and were analyzed by 2-way ANOVA with Tukey’s multiple-comparison test. Survival curves were analyzed by a log-rank (Mantel-Cox) test. Other data are presented as mean ± SEM and were analyzed by 1-way ANOVA.

    Article Snippet: The murine PCa cell line RM-1 was obtained from ATCC.

    Techniques: Adoptive Transfer Assay, Immunofluorescence, In Vivo, Imaging, Western Blot, Expressing, Flow Cytometry, Transduction, In Situ, Comparison

    A Full circle translational research design to explore the immunoregulatory effects of WBM in PCa patients. The initial single‐arm Phase I clinical trial involving WBM tablet consumption (NCT00779168) in PCa patients identified circulating MDSCs as immune cells responsive to WBM treatment. Building upon these findings, the current study includes experiments on PCa murine models and analysis of PCa patients in a dual‐centre, two‐arm, open‐label, randomised Phase II trial (NCT04519879). This bidirectional translational research approach has supported the immunomodulatory role of WBM on MDSCs, thus strengthening the rationale for using WBM as a nutraceutical approach to slow the progression of prostate cancer.

    Journal: Clinical and Translational Medicine

    Article Title: Reduction of myeloid‐derived suppressor cells in prostate cancer murine models and patients following white button mushroom treatment

    doi: 10.1002/ctm2.70048

    Figure Lengend Snippet: A Full circle translational research design to explore the immunoregulatory effects of WBM in PCa patients. The initial single‐arm Phase I clinical trial involving WBM tablet consumption (NCT00779168) in PCa patients identified circulating MDSCs as immune cells responsive to WBM treatment. Building upon these findings, the current study includes experiments on PCa murine models and analysis of PCa patients in a dual‐centre, two‐arm, open‐label, randomised Phase II trial (NCT04519879). This bidirectional translational research approach has supported the immunomodulatory role of WBM on MDSCs, thus strengthening the rationale for using WBM as a nutraceutical approach to slow the progression of prostate cancer.

    Article Snippet: Murine PCa cell lines (TRAMP‐C2 and MyC‐CaP) were purchased from the American Type Culture Collection (ATCC) and were cultured in Dulbecco's modified Eagle's medium (DMEM) with 4 mM L‐glutamine, 1.5 g/L sodium bicarbonate, 4.5 g/L glucose, .005 mg/mL bovine insulin, 10 nM dehydroisoandrosterone, 5% Nu‐Serum IV, 5% fetal bovine serum (FBS), 1% penicillin and 100 μg/mL streptomycin.

    Techniques: Clinical Proteomics

    (A) Three-dimensional and longitudinal cross-sectional μCT images of the tibia from control and RM1 cell administered mice post-IPA-3 treatment. Analysis of trabecular bone (indicated by arrows) demonstrates significant loss of trabecular bone in RM1-injected tibia which was blunted upon treatment with 5 mg/kg/day IPA-3 (n=10). (B-C) A plot showing significantly reduced bone volume percentage and bone marrow density of trabecular area with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days. (D-E) A plot showing the significantly reduced trabecular number with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days (n=10). The trabecular thickness did not change between groups indicating that cancer cells do not affect trabecular thickness in the trabecular section of tibia. Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups. BV=Bone Volume, TV=Tissue Volume, BMD=Bone Marrow Density.

    Journal: Biochemical pharmacology

    Article Title: PAK1 inhibitor IPA-3 mitigates metastatic prostate cancer-induced bone remodeling

    doi: 10.1016/j.bcp.2020.113943

    Figure Lengend Snippet: (A) Three-dimensional and longitudinal cross-sectional μCT images of the tibia from control and RM1 cell administered mice post-IPA-3 treatment. Analysis of trabecular bone (indicated by arrows) demonstrates significant loss of trabecular bone in RM1-injected tibia which was blunted upon treatment with 5 mg/kg/day IPA-3 (n=10). (B-C) A plot showing significantly reduced bone volume percentage and bone marrow density of trabecular area with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days. (D-E) A plot showing the significantly reduced trabecular number with RM1 cell injection into the tibia, which was rescued with IPA-3 treatment for 15 days (n=10). The trabecular thickness did not change between groups indicating that cancer cells do not affect trabecular thickness in the trabecular section of tibia. Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups. BV=Bone Volume, TV=Tissue Volume, BMD=Bone Marrow Density.

    Article Snippet: Cell culture The murine metastatic PCa RM1 cell line (CRL-3310) was obtained from ATCC (Manassas, VA).

    Techniques: Control, Injection

    (A) Representative Western blot images and band densitometry analysis of images showing the PAK1 expression in murine PCa (RM1) cells treated with different doses of IPA-3 for 72 h (n=5). (B) Bar graph showing a dose-dependent reduction in RM1 cell MTT staining by IPA-3 treatment for 72 h (n=6). (C-D) Representative images from the RM1 cell monolayer scratch assay (0 and 24 h) and a bar graph showing the migration of PCa cells in the presence and absence of PAK1 inhibitor IPA-3 after 24 h compared to the DMSO-treated control group (N=5). (E-F) Representative H&E stained lung section images showing a significant decrease in lung colonization in IPA-3 treated group compared to the control group (n=5). Data are presented as mean ± SEM. *p < 0.05; $p < 0.01. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups.

    Journal: Biochemical pharmacology

    Article Title: PAK1 inhibitor IPA-3 mitigates metastatic prostate cancer-induced bone remodeling

    doi: 10.1016/j.bcp.2020.113943

    Figure Lengend Snippet: (A) Representative Western blot images and band densitometry analysis of images showing the PAK1 expression in murine PCa (RM1) cells treated with different doses of IPA-3 for 72 h (n=5). (B) Bar graph showing a dose-dependent reduction in RM1 cell MTT staining by IPA-3 treatment for 72 h (n=6). (C-D) Representative images from the RM1 cell monolayer scratch assay (0 and 24 h) and a bar graph showing the migration of PCa cells in the presence and absence of PAK1 inhibitor IPA-3 after 24 h compared to the DMSO-treated control group (N=5). (E-F) Representative H&E stained lung section images showing a significant decrease in lung colonization in IPA-3 treated group compared to the control group (n=5). Data are presented as mean ± SEM. *p < 0.05; $p < 0.01. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups.

    Article Snippet: Cell culture The murine metastatic PCa RM1 cell line (CRL-3310) was obtained from ATCC (Manassas, VA).

    Techniques: Western Blot, Expressing, Staining, Wound Healing Assay, Migration, Control

    (A) Representative H&E stained images of mouse tibiae showing significantly reduced bone resorption and loss of bone mass induced by RM1 cells in IPA-3-treated mice compared to DMSO control. [Arrows indicate loss of bone mass] (n=10). (B) Bar graph showing the significantly higher percentage of tibia bone area in IPA-3-treated mice compared to the control group (n=10). Data are presented as mean ± SEM. $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups.

    Journal: Biochemical pharmacology

    Article Title: PAK1 inhibitor IPA-3 mitigates metastatic prostate cancer-induced bone remodeling

    doi: 10.1016/j.bcp.2020.113943

    Figure Lengend Snippet: (A) Representative H&E stained images of mouse tibiae showing significantly reduced bone resorption and loss of bone mass induced by RM1 cells in IPA-3-treated mice compared to DMSO control. [Arrows indicate loss of bone mass] (n=10). (B) Bar graph showing the significantly higher percentage of tibia bone area in IPA-3-treated mice compared to the control group (n=10). Data are presented as mean ± SEM. $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups.

    Article Snippet: Cell culture The murine metastatic PCa RM1 cell line (CRL-3310) was obtained from ATCC (Manassas, VA).

    Techniques: Staining, Control

    (A) Control (PBS) and RM1 cell-administered mice post-experiment indicating changes in trabecular bone loss in the presence and absence of IPA-3. Analysis indicated a loss in trabecular mass was significantly inhibited by treatment with 5 mg/kg/day IPA-3 [Arrows indicate the bone loss] (n=10). (B-C) Graphs showing a significant reduction in the loss of tissue volume and bone volume with RM1 cell-injection into the tibia, and its reversal with IPA-3 treatment for 15 days (N=10). Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups.

    Journal: Biochemical pharmacology

    Article Title: PAK1 inhibitor IPA-3 mitigates metastatic prostate cancer-induced bone remodeling

    doi: 10.1016/j.bcp.2020.113943

    Figure Lengend Snippet: (A) Control (PBS) and RM1 cell-administered mice post-experiment indicating changes in trabecular bone loss in the presence and absence of IPA-3. Analysis indicated a loss in trabecular mass was significantly inhibited by treatment with 5 mg/kg/day IPA-3 [Arrows indicate the bone loss] (n=10). (B-C) Graphs showing a significant reduction in the loss of tissue volume and bone volume with RM1 cell-injection into the tibia, and its reversal with IPA-3 treatment for 15 days (N=10). Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups.

    Article Snippet: Cell culture The murine metastatic PCa RM1 cell line (CRL-3310) was obtained from ATCC (Manassas, VA).

    Techniques: Control, Injection

    (A-B) Graphs indicating that while cortical tissue volume was similar in all groups, cortical bone volume was significantly reduced with intra-tibial RM1 cell injection, which was rescued by IPA-3 treatment. This indicates the loss of bone mass induced by cancer cells without affecting tissue volumes in the cortical section of the tibia. (C) Graph showing reduced bone volume percentage with intra-tibial RM1 cells injection, which was rescued with IPA-3 treatment. (D) Graph showing significantly reduced trabecular thickness with intra-tibial RM1 cell injection, which was rescued with IPA-3 treatment. (E) Bar graph showing that there was no change in trabecular number [plate model] between the groups. (N=10). Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups. BV=Bone Volume, TV=Tissue Volume.

    Journal: Biochemical pharmacology

    Article Title: PAK1 inhibitor IPA-3 mitigates metastatic prostate cancer-induced bone remodeling

    doi: 10.1016/j.bcp.2020.113943

    Figure Lengend Snippet: (A-B) Graphs indicating that while cortical tissue volume was similar in all groups, cortical bone volume was significantly reduced with intra-tibial RM1 cell injection, which was rescued by IPA-3 treatment. This indicates the loss of bone mass induced by cancer cells without affecting tissue volumes in the cortical section of the tibia. (C) Graph showing reduced bone volume percentage with intra-tibial RM1 cells injection, which was rescued with IPA-3 treatment. (D) Graph showing significantly reduced trabecular thickness with intra-tibial RM1 cell injection, which was rescued with IPA-3 treatment. (E) Bar graph showing that there was no change in trabecular number [plate model] between the groups. (N=10). Data are presented as mean ± SEM. *p < 0.05; $p < 0.01; #p < 0.001. Unpaired Student’s t-test was used to compare between two groups and One-way ANOVA-Ordinary for more than two groups. BV=Bone Volume, TV=Tissue Volume.

    Article Snippet: Cell culture The murine metastatic PCa RM1 cell line (CRL-3310) was obtained from ATCC (Manassas, VA).

    Techniques: Injection