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MedChemExpress lncap enz cells
Lncap Enz Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 278 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lncap+enz+cells/Enzalutamide/pm41151858-65-3-11
Average 98 stars, based on 278 article reviews

lncap enz cells - by Bioz Stars, 2026-09

98/100 stars

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Cell Culture:

Article Title: SCAMP3 and EPS8 Cooperatively Regulate EGFR Signaling to Promote Enzalutamide Resistance and Metastatic Potential in Prostate Cancer.
Article Snippet: LNCap prostate cancer cells (ATCC® CRL‐1740TM) and their enzalutamide‐ resistant derivative LNCap‐Enz were maintained in DMEM medium supplemented with 10% fetal bovine serum (FBS) and 2% penicillin/streptomycin. .. For resistance maintenance, LNCap‐Enz cells were cultured with 10 μM enzalutamide (MedChem Express, MDV3100, Monmouth Junction, NJ, USA). ..

Article Title: SCAMP3 and EPS8 Cooperatively Regulate EGFR Signaling to Promote Enzalutamide Resistance and Metastatic Potential in Prostate Cancer
Article Snippet: LNCap prostate cancer cells (ATCC ® CRL-1740TM) and their enzalutamide-resistant derivative LNCap-Enz were maintained in DMEM medium supplemented with 10% fetal bovine serum (FBS) and 2% penicillin/streptomycin. .. For resistance maintenance, LNCap-Enz cells were cultured with 10 μM enzalutamide (MedChem Express, MDV3100, Monmouth Junction, NJ, USA). ..

Image Search Results

Rutin reduces cell viability in prostate cancer cell lines. Cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h, and cell viability was assessed by the MTT assay. (A) PC3, (B) DU145, (C) LNCaP, and (D) enzalutamide-resistant LNCaP-Enz cells were evaluated. Data are presented as the mean±SD from three independent experiments. *p<0.05 compared to untreated control, using one-way ANOVA followed by Tukey’s post hoc test. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; SD: standard deviation.

Journal: Cancer Genomics & Proteomics

Article Title: Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate Cancer Cells

doi: 10.21873/cgp.20550

Figure Lengend Snippet: Rutin reduces cell viability in prostate cancer cell lines. Cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h, and cell viability was assessed by the MTT assay. (A) PC3, (B) DU145, (C) LNCaP, and (D) enzalutamide-resistant LNCaP-Enz cells were evaluated. Data are presented as the mean±SD from three independent experiments. *p<0.05 compared to untreated control, using one-way ANOVA followed by Tukey’s post hoc test. MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; SD: standard deviation.

Article Snippet: Enzalutamide-resistant LNCaP cells (LNCaP-Enz) were established by continuous exposure of parental LNCaP cells to 10 μM enzalutamide (Selleck Chemicals, Houston, TX, USA) for over 6 months.

Techniques: MTT Assay, Control, Standard Deviation

Rutin modulates the EMT markers in prostate cancer cells. (A, B) PC3 cells, (C, D) DU145 cells, (E, F) LNCaP cells, and (G, H) LNCaP-Enz cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h. Protein expression levels of E-cadherin, α-SMA, Snail, and Slug were evaluated by Western blotting. β-actin was used as a loading control. Representative Western blot images are shown in (A), (C), (E), and (G), and densitometric quantifications normalized to β-actin are presented in (B), (D), (F), and (H). Rutin treatment induced a concentration-dependent increase in E-cadherin expression and a decrease in α-SMA, Snail, and Slug levels across all cell lines, with the most pronounced effects observed in enzalutamide-resistant LNCaP-Enz cells. Quantitative data represent the mean±SD from three independent experiments. *p<0.05 vs. control using one-way ANOVA followed by Tukey’s post hoc test. EMT: epithelial–mesenchymal transition; α-SMA: α-smooth muscle actin; SD: standard deviation.

Journal: Cancer Genomics & Proteomics

Article Title: Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate Cancer Cells

doi: 10.21873/cgp.20550

Figure Lengend Snippet: Rutin modulates the EMT markers in prostate cancer cells. (A, B) PC3 cells, (C, D) DU145 cells, (E, F) LNCaP cells, and (G, H) LNCaP-Enz cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h. Protein expression levels of E-cadherin, α-SMA, Snail, and Slug were evaluated by Western blotting. β-actin was used as a loading control. Representative Western blot images are shown in (A), (C), (E), and (G), and densitometric quantifications normalized to β-actin are presented in (B), (D), (F), and (H). Rutin treatment induced a concentration-dependent increase in E-cadherin expression and a decrease in α-SMA, Snail, and Slug levels across all cell lines, with the most pronounced effects observed in enzalutamide-resistant LNCaP-Enz cells. Quantitative data represent the mean±SD from three independent experiments. *p<0.05 vs. control using one-way ANOVA followed by Tukey’s post hoc test. EMT: epithelial–mesenchymal transition; α-SMA: α-smooth muscle actin; SD: standard deviation.

Techniques: Expressing, Western Blot, Control, Concentration Assay, Standard Deviation

Rutin enhances mitochondrial biogenesis in prostate cancer cells. Cells were treated with rutin (0, 25, 50, and 100 μM) for 24 h, and mitochondrial biogenesis was assessed using the MitoBiogenesis™ In-Cell ELISA Kit. The assay measures mitochondrially encoded COX-I and nuclear-encoded SDHA as indicators of mitochondrial content. (A) PC3, (B) DU145, (C) LNCaP, and (D) LNCaP-Enz cells were analyzed. The mitochondrial biogenesis index was calculated as the ratio of COX-I to SDHA absorbance. Rutin increased mitochondrial biogenesis in a dose-dependent manner, with the most substantial effect observed in LNCaP-Enz cells. Data represent the mean±SD of three independent experiments. Statistical significance was determined by two-way repeated measures ANOVA followed by the Holm–Šidák post hoc test. *p<0.05 vs. vehicle at the same time point. SD: Standard deviation.

Journal: Cancer Genomics & Proteomics

Article Title: Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate Cancer Cells

doi: 10.21873/cgp.20550

Figure Lengend Snippet: Rutin enhances mitochondrial biogenesis in prostate cancer cells. Cells were treated with rutin (0, 25, 50, and 100 μM) for 24 h, and mitochondrial biogenesis was assessed using the MitoBiogenesis™ In-Cell ELISA Kit. The assay measures mitochondrially encoded COX-I and nuclear-encoded SDHA as indicators of mitochondrial content. (A) PC3, (B) DU145, (C) LNCaP, and (D) LNCaP-Enz cells were analyzed. The mitochondrial biogenesis index was calculated as the ratio of COX-I to SDHA absorbance. Rutin increased mitochondrial biogenesis in a dose-dependent manner, with the most substantial effect observed in LNCaP-Enz cells. Data represent the mean±SD of three independent experiments. Statistical significance was determined by two-way repeated measures ANOVA followed by the Holm–Šidák post hoc test. *p<0.05 vs. vehicle at the same time point. SD: Standard deviation.

Techniques: In-Cell ELISA, Standard Deviation

Rutin activates the AMPK–SIRT1–PGC1α–NRF1–TFAM signaling axis in prostate cancer cells. (A, B) PC3 cells, (C, D) DU145 cells, (E, F) LNCaP cells, and (G, H) LNCaP-Enz cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h. Protein expression levels of AMPK, SIRT1, PGC1α, NRF1, and TFAM were assessed by Western blotting, with β-actin serving as the loading control. Representative Western blot images are shown in (A), (C), (E), and (G), and corresponding densitometric quantifications normalized to β-actin are presented in (B), (D), (F), and (H). Rutin treatment resulted in a dose-dependent up-regulation of AMPK, SIRT1, PGC1α, NRF1, and TFAM expression across all prostate cancer cell lines, with the most pronounced effects observed in enzalutamide-resistant LNCaP-Enz cells. Quantitative data are expressed as mean±SD from three independent experiments. Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. *p<0.05 vs. control. AMPK: AMP-activated protein kinase; SIRT1-Sirtuin 1: NAD⁺-dependent deacetylase sirtuin-1; PGC-1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; NRF1: nuclear respiratory factor 1; TFAM: transcription factor A, mitochondrial; SD: standard deviation.

Journal: Cancer Genomics & Proteomics

Article Title: Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate Cancer Cells

doi: 10.21873/cgp.20550

Figure Lengend Snippet: Rutin activates the AMPK–SIRT1–PGC1α–NRF1–TFAM signaling axis in prostate cancer cells. (A, B) PC3 cells, (C, D) DU145 cells, (E, F) LNCaP cells, and (G, H) LNCaP-Enz cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h. Protein expression levels of AMPK, SIRT1, PGC1α, NRF1, and TFAM were assessed by Western blotting, with β-actin serving as the loading control. Representative Western blot images are shown in (A), (C), (E), and (G), and corresponding densitometric quantifications normalized to β-actin are presented in (B), (D), (F), and (H). Rutin treatment resulted in a dose-dependent up-regulation of AMPK, SIRT1, PGC1α, NRF1, and TFAM expression across all prostate cancer cell lines, with the most pronounced effects observed in enzalutamide-resistant LNCaP-Enz cells. Quantitative data are expressed as mean±SD from three independent experiments. Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. *p<0.05 vs. control. AMPK: AMP-activated protein kinase; SIRT1-Sirtuin 1: NAD⁺-dependent deacetylase sirtuin-1; PGC-1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; NRF1: nuclear respiratory factor 1; TFAM: transcription factor A, mitochondrial; SD: standard deviation.

Techniques: Expressing, Western Blot, Control, Histone Deacetylase Assay, Standard Deviation

Rutin activates the PERK–ATF6 signaling axis in prostate cancer cells. PC3 (A, B), DU145 (C, D), LNCaP (E, F), and LNCaP-Enz (G, H) cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h. Protein expression levels of PERK and ATF6 were evaluated by Western blot analysis. β-actin was used as a loading control. Representative Western blot images are shown in (A), (C), (E), and (G), and densitometric quantifications normalized to β-actin are shown in (B), (D), (F), and (H). In PC3 and DU145 cells, PERK expression increased in a dose-dependent manner, while ATF6 up-regulation was evident primarily at higher concentrations. In LNCaP and LNCaP-Enz cells, both PERK and ATF6 were strongly induced even at lower doses, indicating a heightened sensitivity to rutin-induced ER stress signaling. These findings suggest that rutin enhances ER stress responses via the PERK–ATF6 pathway and may promote mitochondrial–ER communication, particularly in hormone-sensitive and drug-resistant prostate cancer cells. Quantitative data are presented as mean±SD from three independent experiments. Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. p<0.05 vs. control. Protein expression levels of protein kinase RNA-like endoplasmic reticulum kinase: PERK: Protein kinase RNA-like endoplasmic reticulum kinase; ATF6: activating transcription factor 6; SD: standard deviation.

Journal: Cancer Genomics & Proteomics

Article Title: Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate Cancer Cells

doi: 10.21873/cgp.20550

Figure Lengend Snippet: Rutin activates the PERK–ATF6 signaling axis in prostate cancer cells. PC3 (A, B), DU145 (C, D), LNCaP (E, F), and LNCaP-Enz (G, H) cells were treated with increasing concentrations of rutin (0, 25, 50, and 100 μM) for 24 h. Protein expression levels of PERK and ATF6 were evaluated by Western blot analysis. β-actin was used as a loading control. Representative Western blot images are shown in (A), (C), (E), and (G), and densitometric quantifications normalized to β-actin are shown in (B), (D), (F), and (H). In PC3 and DU145 cells, PERK expression increased in a dose-dependent manner, while ATF6 up-regulation was evident primarily at higher concentrations. In LNCaP and LNCaP-Enz cells, both PERK and ATF6 were strongly induced even at lower doses, indicating a heightened sensitivity to rutin-induced ER stress signaling. These findings suggest that rutin enhances ER stress responses via the PERK–ATF6 pathway and may promote mitochondrial–ER communication, particularly in hormone-sensitive and drug-resistant prostate cancer cells. Quantitative data are presented as mean±SD from three independent experiments. Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. p<0.05 vs. control. Protein expression levels of protein kinase RNA-like endoplasmic reticulum kinase: PERK: Protein kinase RNA-like endoplasmic reticulum kinase; ATF6: activating transcription factor 6; SD: standard deviation.

Techniques: Expressing, Western Blot, Control, Standard Deviation

ER stress inhibition attenuates rutin-induced EMT suppression and metabolic activation in prostate cancer cells. Western blot analysis of E-cadherin, α-SMA, IRE1, PERK, AMPK, and SIRT1 expression in PC3 (A, B), DU145 (C, D), LNCaP (E, F), and LNCaP-Enz (G, H) cells following 24-h treatment with rutin (100 μM), either alone or in combination with TUDCA (100 μM; chemical chaperone that alleviates ER stress) or Salubrinal (200 nM; an inhibitor of eIF2α dephosphorylation functioning as a modulator of UPR signaling). β-actin was used as the internal loading control. Representative Western blot images are presented in (A), (C), (E), (G), and corresponding densitometric quantifications normalized to β-actin are shown in (B), (D), (F), (H). Rutin treatment increased E-cadherin and up-regulated PERK, IRE1, AMPK, and SIRT1 expression while decreasing α-SMA across all cell lines. Co-treatment with ER stress inhibitors partially reversed these effects, particularly in LNCaP-Enz cells, indicating that rutin’s anti-EMT and metabolic actions are mediated in part through ER stress-dependent signaling. Quantitative data are expressed as mean±SD from three independent experiments. Statistical significance was assessed by one-way ANOVA followed by Tukey’s post hoc test (*p<0.05 vs. the untreated control group; # p<0.05 compared with the rutin-treated group). TUDCA: Tauroursodeoxycholic acid; SD: standard deviation.

Journal: Cancer Genomics & Proteomics

Article Title: Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate Cancer Cells

doi: 10.21873/cgp.20550

Figure Lengend Snippet: ER stress inhibition attenuates rutin-induced EMT suppression and metabolic activation in prostate cancer cells. Western blot analysis of E-cadherin, α-SMA, IRE1, PERK, AMPK, and SIRT1 expression in PC3 (A, B), DU145 (C, D), LNCaP (E, F), and LNCaP-Enz (G, H) cells following 24-h treatment with rutin (100 μM), either alone or in combination with TUDCA (100 μM; chemical chaperone that alleviates ER stress) or Salubrinal (200 nM; an inhibitor of eIF2α dephosphorylation functioning as a modulator of UPR signaling). β-actin was used as the internal loading control. Representative Western blot images are presented in (A), (C), (E), (G), and corresponding densitometric quantifications normalized to β-actin are shown in (B), (D), (F), (H). Rutin treatment increased E-cadherin and up-regulated PERK, IRE1, AMPK, and SIRT1 expression while decreasing α-SMA across all cell lines. Co-treatment with ER stress inhibitors partially reversed these effects, particularly in LNCaP-Enz cells, indicating that rutin’s anti-EMT and metabolic actions are mediated in part through ER stress-dependent signaling. Quantitative data are expressed as mean±SD from three independent experiments. Statistical significance was assessed by one-way ANOVA followed by Tukey’s post hoc test (*p<0.05 vs. the untreated control group; # p<0.05 compared with the rutin-treated group). TUDCA: Tauroursodeoxycholic acid; SD: standard deviation.

Techniques: Inhibition, Activation Assay, Western Blot, Expressing, De-Phosphorylation Assay, Control, Standard Deviation

PAX6 expression is upregulated in NEPC. a Intersection of differentially expressed genes from the NEPC related datasets. b The expression of PAX6 in NEPC patients based on GSE137829 dataset (P2, patient 2; P4, patient 4; P5, patient 5; P6, patient 6). c Comparisons of PAX6 mRNA levels level in CRPC-Adeno and NEPC based on the GSE32967 dataset (CRPC-Adeno, n = 8; NEPC, n = 14). d Comparisons of PAX6 mRNA levels in CRPC-Adeno vs. CRPC-NE based on the Beltran-2016 dataset (CRPC-Adeno, n = 35; CRPC-NE, n = 15). e Comparisons of PAX6 mRNA levels in HSPC vs. HRPC based on GSE6752 dataset (HSPC, n = 10; HRPC, n = 21). f Correlation analysis of PAX6 with NE signature genes based on the Beltran 2016 Cohort. g Correlation analysis of PAX6 with NE signature genes based on the Broad/Cornell 2012 Cohort. h Correlation analysis of PAX6 with AR associated genes based on the Beltran 2016 Cohort. i Correlation analysis of PAX6 with AR associated genes based on the Broad/Cornell 2012 Cohort. j Representative H&E and IHC staining of PAX6, AR and SYP in tissues from patients with Primary PCa, CRPC or NEPC (Scale Bar: 100 μm). k Protein expression of PAX6 in PCa cell lines. l Protein and mRNA expression of PAX6 in LNCaP ENZ cells compared to the control cells. All the experiments were repeated for three times. Data represents the mean ± SD, *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: PAX6 expression is upregulated in NEPC. a Intersection of differentially expressed genes from the NEPC related datasets. b The expression of PAX6 in NEPC patients based on GSE137829 dataset (P2, patient 2; P4, patient 4; P5, patient 5; P6, patient 6). c Comparisons of PAX6 mRNA levels level in CRPC-Adeno and NEPC based on the GSE32967 dataset (CRPC-Adeno, n = 8; NEPC, n = 14). d Comparisons of PAX6 mRNA levels in CRPC-Adeno vs. CRPC-NE based on the Beltran-2016 dataset (CRPC-Adeno, n = 35; CRPC-NE, n = 15). e Comparisons of PAX6 mRNA levels in HSPC vs. HRPC based on GSE6752 dataset (HSPC, n = 10; HRPC, n = 21). f Correlation analysis of PAX6 with NE signature genes based on the Beltran 2016 Cohort. g Correlation analysis of PAX6 with NE signature genes based on the Broad/Cornell 2012 Cohort. h Correlation analysis of PAX6 with AR associated genes based on the Beltran 2016 Cohort. i Correlation analysis of PAX6 with AR associated genes based on the Broad/Cornell 2012 Cohort. j Representative H&E and IHC staining of PAX6, AR and SYP in tissues from patients with Primary PCa, CRPC or NEPC (Scale Bar: 100 μm). k Protein expression of PAX6 in PCa cell lines. l Protein and mRNA expression of PAX6 in LNCaP ENZ cells compared to the control cells. All the experiments were repeated for three times. Data represents the mean ± SD, *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Expressing, Immunohistochemistry, Control

Elevated expression of PAX6 is associated with the resistance to ENZ in PCa. a Relative mRNA expression of NE signature genes and AR associated genes in LNCaP ENZ cells compared with the control by RNA-seq. b GSEA results of the indicated gene signatures for the comparisons of LNCaP ENZ and control cells. c mRNA expression of NE signature genes in LNCaP ENZ and control cells. d mRNA expression of AR associated genes in LNCaP ENZ and control cells. e Protein expression of SYP, NSE, KLK3, AR in LNCaP ENZ cells and control cells. f Protein expression of PAX6, NSE, CHGA, SYP and NCAM1 in LNCaP ENZ -sh PAX6 cells and control cells. g Cell proliferation assays in LNCaP ENZ -sh PAX6 cells and control cells. Data represent the fold change of OD value during an observation period of up to 4 days. Fold change on the day of cell seeding (day0) in each group was set as 1. h Representative image and quantification assay of colony numbers in LNCaP ENZ -sh PAX6 cells and control cells. i Representative image and quantification assay of tumorsphere formation in LNCaP ENZ -sh PAX6 cells and control cells. j Flow cytometric analysis for cell apoptosis by the percentage of Annexin V + cell population in LNCaP ENZ -sh PAX6 cells and control cells. All the experiments were repeated for three times. Data represents the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: Elevated expression of PAX6 is associated with the resistance to ENZ in PCa. a Relative mRNA expression of NE signature genes and AR associated genes in LNCaP ENZ cells compared with the control by RNA-seq. b GSEA results of the indicated gene signatures for the comparisons of LNCaP ENZ and control cells. c mRNA expression of NE signature genes in LNCaP ENZ and control cells. d mRNA expression of AR associated genes in LNCaP ENZ and control cells. e Protein expression of SYP, NSE, KLK3, AR in LNCaP ENZ cells and control cells. f Protein expression of PAX6, NSE, CHGA, SYP and NCAM1 in LNCaP ENZ -sh PAX6 cells and control cells. g Cell proliferation assays in LNCaP ENZ -sh PAX6 cells and control cells. Data represent the fold change of OD value during an observation period of up to 4 days. Fold change on the day of cell seeding (day0) in each group was set as 1. h Representative image and quantification assay of colony numbers in LNCaP ENZ -sh PAX6 cells and control cells. i Representative image and quantification assay of tumorsphere formation in LNCaP ENZ -sh PAX6 cells and control cells. j Flow cytometric analysis for cell apoptosis by the percentage of Annexin V + cell population in LNCaP ENZ -sh PAX6 cells and control cells. All the experiments were repeated for three times. Data represents the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Expressing, Control, RNA Sequencing

Knockdown of PAX6 represses the phenotype of NEPC. a Protein expression of PAX6 and NSE after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. b Cell proliferation assay after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. c Representative image and quantification assay of tumorsphere formation after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. d Representative image and quantification assay of colony formation after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. e Protein expression of PAX6 and NSE in DU145-sh PAX6 cells and control cells. f Cell proliferation assays in DU145-sh PAX6 cells and control cells. g Representative image and quantification assay of tumorsphere formation after PAX6 knockdown in DU145-sh PAX6 cells and control cells. h Representative image and quantification assay of colony formation in DU145-sh PAX6 cells and control cells. i Graphic of the construction of the xenograft model in castrated nude mice. j Anatomic tumor image of DU145-sh PAX6 cells or control cells inoculated xenografts. k Tumor volume analysis of DU145-sh PAX6 cells and control cells inoculated xenografts at the end point. l Tumor weight analysis of DU145-sh PAX6 cells and control cells inoculated xenografts. m Representative H&E staining and IHC staining of Ki67, PAX6, SYP in xenograft samples (Scale Bar: 100 μm, with the boxed region enlarged and shown on the left). All the experiments were repeated for three times. Data represents the mean ± SD.* p < 0.05, ** p < 0.01, *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: Knockdown of PAX6 represses the phenotype of NEPC. a Protein expression of PAX6 and NSE after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. b Cell proliferation assay after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. c Representative image and quantification assay of tumorsphere formation after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. d Representative image and quantification assay of colony formation after PAX6 knockdown in LNCaP-sh RB1/TP53 cells and control cells. e Protein expression of PAX6 and NSE in DU145-sh PAX6 cells and control cells. f Cell proliferation assays in DU145-sh PAX6 cells and control cells. g Representative image and quantification assay of tumorsphere formation after PAX6 knockdown in DU145-sh PAX6 cells and control cells. h Representative image and quantification assay of colony formation in DU145-sh PAX6 cells and control cells. i Graphic of the construction of the xenograft model in castrated nude mice. j Anatomic tumor image of DU145-sh PAX6 cells or control cells inoculated xenografts. k Tumor volume analysis of DU145-sh PAX6 cells and control cells inoculated xenografts at the end point. l Tumor weight analysis of DU145-sh PAX6 cells and control cells inoculated xenografts. m Representative H&E staining and IHC staining of Ki67, PAX6, SYP in xenograft samples (Scale Bar: 100 μm, with the boxed region enlarged and shown on the left). All the experiments were repeated for three times. Data represents the mean ± SD.* p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Knockdown, Expressing, Control, Proliferation Assay, Staining, Immunohistochemistry

Over-expression of PAX6 promotes the NE trans-differentiation in non-NEPC cells. a mRNA and protein expression of PAX6 in LNCaP- PAX6 cells and control cells. b mRNA and protein expression of SYP and ENO2 genes in LNCaP- PAX6 cells and control cells. c Cell proliferation assays in LNCaP- PAX6 cells and control cells after treatment of ENZ (20 µM). d Representative image and quantification assay of colony number in LNCaP- PAX6 cells and control cells. e Representative image and quantification assay of tumorsphere formation in LNCaP- PAX6 cells and control cells. f ENZ dose–response curves for LNCaP- PAX6 cells and control cells. All the experiments were repeated for three times. Data represents the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: Over-expression of PAX6 promotes the NE trans-differentiation in non-NEPC cells. a mRNA and protein expression of PAX6 in LNCaP- PAX6 cells and control cells. b mRNA and protein expression of SYP and ENO2 genes in LNCaP- PAX6 cells and control cells. c Cell proliferation assays in LNCaP- PAX6 cells and control cells after treatment of ENZ (20 µM). d Representative image and quantification assay of colony number in LNCaP- PAX6 cells and control cells. e Representative image and quantification assay of tumorsphere formation in LNCaP- PAX6 cells and control cells. f ENZ dose–response curves for LNCaP- PAX6 cells and control cells. All the experiments were repeated for three times. Data represents the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Over Expression, Expressing, Control

The expression of PAX6 is negatively regulated by AR . a Correlation analysis of PAX6 with AR expression based on the MD Anderson, 2023 Cohort. b Correlation analysis of PAX6 with AR expression based on the Gao, 2014 Cohort. c Correlation analysis of PAX6 with AR expression based on the SU2C/PCF 2019 Cohort. d Genomic browser representation of AR binding in PAX6 promoter region encompassing an ARE by analysis of the data from GSE161167 (LNCaP cells) and GSE56288 (a cohort of normal and tumor human prostate tissues) datasets. e mRNA expression of PAX6 , SYP, ENO2 and STEAP4 in LNCaP cells after treatment with R1881 (1 nM) for 6 h. f mRNA and protein expression of PAX6 and AR after AR knockdown in LNCaP cells. g protein expression of PAX6 and AR after AR knockout in LNCaP cells. h ChIP assay of AR binding at region of the P1 promoter region of PAX6 after treatment with DHT (10 nM) in LNCaP cells. i Determination of PAX6 ARE-luc activity after treatment with R1881(1 nM, 6 h) or R1881 (1 nM, 6 h) + ENZ (20 µM, 6 h) in LNCaP cells. j mRNA and protein expression of AR and KLK3 in LNCaP- PAX6 and control cells. k mRNA and protein expression of AR and KLK3 in C42B- PAX6 and control cells. l ChIP assay of PAX6 binding at the promoter region of AR. All the experiments were repeated for three times. Data represents the mean ± SD. ns: no significance, ** p < 0.01, *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: The expression of PAX6 is negatively regulated by AR . a Correlation analysis of PAX6 with AR expression based on the MD Anderson, 2023 Cohort. b Correlation analysis of PAX6 with AR expression based on the Gao, 2014 Cohort. c Correlation analysis of PAX6 with AR expression based on the SU2C/PCF 2019 Cohort. d Genomic browser representation of AR binding in PAX6 promoter region encompassing an ARE by analysis of the data from GSE161167 (LNCaP cells) and GSE56288 (a cohort of normal and tumor human prostate tissues) datasets. e mRNA expression of PAX6 , SYP, ENO2 and STEAP4 in LNCaP cells after treatment with R1881 (1 nM) for 6 h. f mRNA and protein expression of PAX6 and AR after AR knockdown in LNCaP cells. g protein expression of PAX6 and AR after AR knockout in LNCaP cells. h ChIP assay of AR binding at region of the P1 promoter region of PAX6 after treatment with DHT (10 nM) in LNCaP cells. i Determination of PAX6 ARE-luc activity after treatment with R1881(1 nM, 6 h) or R1881 (1 nM, 6 h) + ENZ (20 µM, 6 h) in LNCaP cells. j mRNA and protein expression of AR and KLK3 in LNCaP- PAX6 and control cells. k mRNA and protein expression of AR and KLK3 in C42B- PAX6 and control cells. l ChIP assay of PAX6 binding at the promoter region of AR. All the experiments were repeated for three times. Data represents the mean ± SD. ns: no significance, ** p < 0.01, *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Expressing, Binding Assay, Knockdown, Knock-Out, Activity Assay, Control

PAX6 promotes NE characteristics via STAT5A . a The heatmap of candidate TFs with significant expressional difference in DU145-sh PAX6 cells and DU145-Scramble cells. b Comparisons of STAT5A mRNA expression in CRPC-Adeno vs. NEPC based on the GSE32967 dataset (CRPC-Adeno, n = 8; NEPC, n = 14). c Representative IHC staining of STAT5A in tissues from patient with Primary PCa, CRPC or NEPC (Scale Bar: 100 μm). d ChIP assay of PAX6 binding at the promoter region of STAT5A in LNCaP- PAX6 cells. e Protein expression of PAX6, STAT5A, SYP and NSE in DU145-sh PAX6 cells with or without STAT5A overexpression. f Cell proliferation assay in DU145-sh PAX6 cells with or without STAT5A overexpression. g Representative image and quantification assay of tumorsphere formation in DU145-sh PAX6 cells with or without STAT5A over-expression. h Anatomic tumor images and tumor weight analysis of DU145-sh PAX6 cells inoculated xenografts with or without STAT5A overexpression ( n = 6). i Tumor volume analysis of DU145-Scramble, DU145-sh PAX6 or DU145-sh PAX6 + STAT5A cells inoculated xenografts respectively ( n = 6). j Tumor weights analysis of DU145-sh PAX6 and DU145-sh PAX6 + STAT5A cells inoculated xenografts respectively ( n = 6). k Representative staining H&E and IHC staining of PAX6, Ki67, SYP, NSE, NCAM1 in DU145-sh PAX6 and DU145-sh PAX6 + STAT5A cells inoculated xenograft samples (Scale Bar: 100 μm, with the boxed region enlarged and shown on the left, n = 6). All the experiments were repeated for three times. Data represents the mean ± SD. ns: no significance, * p < 0.05, *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: PAX6 promotes NE characteristics via STAT5A . a The heatmap of candidate TFs with significant expressional difference in DU145-sh PAX6 cells and DU145-Scramble cells. b Comparisons of STAT5A mRNA expression in CRPC-Adeno vs. NEPC based on the GSE32967 dataset (CRPC-Adeno, n = 8; NEPC, n = 14). c Representative IHC staining of STAT5A in tissues from patient with Primary PCa, CRPC or NEPC (Scale Bar: 100 μm). d ChIP assay of PAX6 binding at the promoter region of STAT5A in LNCaP- PAX6 cells. e Protein expression of PAX6, STAT5A, SYP and NSE in DU145-sh PAX6 cells with or without STAT5A overexpression. f Cell proliferation assay in DU145-sh PAX6 cells with or without STAT5A overexpression. g Representative image and quantification assay of tumorsphere formation in DU145-sh PAX6 cells with or without STAT5A over-expression. h Anatomic tumor images and tumor weight analysis of DU145-sh PAX6 cells inoculated xenografts with or without STAT5A overexpression ( n = 6). i Tumor volume analysis of DU145-Scramble, DU145-sh PAX6 or DU145-sh PAX6 + STAT5A cells inoculated xenografts respectively ( n = 6). j Tumor weights analysis of DU145-sh PAX6 and DU145-sh PAX6 + STAT5A cells inoculated xenografts respectively ( n = 6). k Representative staining H&E and IHC staining of PAX6, Ki67, SYP, NSE, NCAM1 in DU145-sh PAX6 and DU145-sh PAX6 + STAT5A cells inoculated xenograft samples (Scale Bar: 100 μm, with the boxed region enlarged and shown on the left, n = 6). All the experiments were repeated for three times. Data represents the mean ± SD. ns: no significance, * p < 0.05, *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Expressing, Immunohistochemistry, Binding Assay, Over Expression, Proliferation Assay, Staining

PAX6 promotes the expression of MET to further phosphorylate STAT5A. a Protein expression of MET, p-MET, STAT5A and p-STAT5A after stimulation with different concentrations of HGF in LNCaP and C42B cells. b Protein expression of MET, p-MET, STAT5A and p-STAT5A after stimulation with different concentrations of HGF in MET -knockdown or the control LNCaP cells. c Representative IHC staining of MET in tissues from patients with Primary PCa, CRPC or NEPC. d Correlation analysis of MET with PAX6 expression based on the GSE21034 dataset, TCGA database and the Fred Hutchinson, 2016 Cohort. e Correlation analysis of the expression of MET and NE signature genes based on the Broad 2012 Cohort. f mRNA and protein expression of MET in DU145-sh PAX6 cells and control cells. g mRNA and protein expression of MET in PC3-sh PAX6 cells and control cells. h Representative IHC staining of MET and p-MET in DU145-sh PAX6 and PC3-sh PAX6 compared with control cells inoculated xenograft samples (Scale Bar: 100 μm, with the boxed region enlarged and shown on the left). i ChIP assay of PAX6 binding at regions of the MET promoter in LNCaP cells. All the experiments were repeated for three times. Data represents the mean ± SD. *** p < 0.001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: PAX6 promotes the expression of MET to further phosphorylate STAT5A. a Protein expression of MET, p-MET, STAT5A and p-STAT5A after stimulation with different concentrations of HGF in LNCaP and C42B cells. b Protein expression of MET, p-MET, STAT5A and p-STAT5A after stimulation with different concentrations of HGF in MET -knockdown or the control LNCaP cells. c Representative IHC staining of MET in tissues from patients with Primary PCa, CRPC or NEPC. d Correlation analysis of MET with PAX6 expression based on the GSE21034 dataset, TCGA database and the Fred Hutchinson, 2016 Cohort. e Correlation analysis of the expression of MET and NE signature genes based on the Broad 2012 Cohort. f mRNA and protein expression of MET in DU145-sh PAX6 cells and control cells. g mRNA and protein expression of MET in PC3-sh PAX6 cells and control cells. h Representative IHC staining of MET and p-MET in DU145-sh PAX6 and PC3-sh PAX6 compared with control cells inoculated xenograft samples (Scale Bar: 100 μm, with the boxed region enlarged and shown on the left). i ChIP assay of PAX6 binding at regions of the MET promoter in LNCaP cells. All the experiments were repeated for three times. Data represents the mean ± SD. *** p < 0.001

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Expressing, Knockdown, Control, Immunohistochemistry, Binding Assay

PAX6 induced the change of lineage plasticity by attenuating the H4K20me3. a The heatmap showing the average ATAC-Seq signal centered on the TSS of the nearest genes in LNCaP- PAX6 , LNCaP- STAT5A and control cells. b Chromatin accessibility of ENO2, CHGA , SYP , NCAM1, MYCN and ASCL1 in LNCaP- PAX6 or LNCaP- STAT5A cells compared with that in the control cells. c GO analysis showing the top 5 increased and decreased biological process in LNCaP- PAX6 vs. the control cells. d Protein expression of SMYD5 and KMT5C in LNCaP- PAX6 cells with or without knockdown of STAT5A . e Protein expression of SMYD5 and KMT5C in DU145-sh PAX6 cells with or without overexpression of STAT5A . f Protein expression of KMT5C and STAT5A in DU145-sh PAX6 and PC3-sh PAX6 cells. g Graphic summary of this study

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: PAX6 promotes neuroendocrine phenotypes of prostate cancer via enhancing MET/STAT5A-mediated chromatin accessibility

doi: 10.1186/s13046-024-03064-1

Figure Lengend Snippet: PAX6 induced the change of lineage plasticity by attenuating the H4K20me3. a The heatmap showing the average ATAC-Seq signal centered on the TSS of the nearest genes in LNCaP- PAX6 , LNCaP- STAT5A and control cells. b Chromatin accessibility of ENO2, CHGA , SYP , NCAM1, MYCN and ASCL1 in LNCaP- PAX6 or LNCaP- STAT5A cells compared with that in the control cells. c GO analysis showing the top 5 increased and decreased biological process in LNCaP- PAX6 vs. the control cells. d Protein expression of SMYD5 and KMT5C in LNCaP- PAX6 cells with or without knockdown of STAT5A . e Protein expression of SMYD5 and KMT5C in DU145-sh PAX6 cells with or without overexpression of STAT5A . f Protein expression of KMT5C and STAT5A in DU145-sh PAX6 and PC3-sh PAX6 cells. g Graphic summary of this study

Article Snippet: LNCaP ENZ cell line was cultured further in the continuous presence of 20 μM ENZ (Med Chem Express, Shanghai, China) to maintain ENZ resistance.

Techniques: Control, Expressing, Knockdown, Over Expression

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