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col1a1 overexpression constructs  (Genechem)

 
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    Genechem col1a1 overexpression constructs
    ADAMTS2 is coexpressed and physically interacts with <t>COL1A1</t> in PCa. (A) Heatmap of the top 10 genes most strongly related to ADAMTS2 expression in the TCGA-PRAD cohort. (B) Scatter plot showing the correlation between ADAMTS2 and COL1A1 mRNA levels. (C) PPI network prediction from the STRING database indicating a potential interaction between ADAMTS2 and COL1A1. (D, E) Validation of COL1A1 mRNA ( n =6 pairs) and protein ( n =3 pairs) levels in paired human PCa and adjacent non-tumoral tissues using qRT-PCR and WB (paired two-tailed Student’s t-test). (F, G) Reciprocal Co-IP assessments illustrating physical interaction between endogenous and exogenously expressed ADAMTS2 and COL1A1 in DU145 cells. (H) WB of COL1A1 protein levels upon ADAMTS2 overexpression or knockdown in DU145 cells. (I) Evaluation of COL1A1 upregulation and downregulation effectiveness by WB in DU145 cells. Representative images from three independent experiments are shown. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3; unpaired two-tailed Student’s t-test). *P < 0.05, ***P < 0.001.
    Col1a1 Overexpression Constructs, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/shrna+construct/constructs+overexpression/pmc13158085-52-6-23
    Average 86 stars, based on 1 article reviews
    col1a1 overexpression constructs - by Bioz Stars, 2026-09
    86/100 stars

    Images

    1) Product Images from "ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1"

    Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2026.1784882

    ADAMTS2 is coexpressed and physically interacts with COL1A1 in PCa. (A) Heatmap of the top 10 genes most strongly related to ADAMTS2 expression in the TCGA-PRAD cohort. (B) Scatter plot showing the correlation between ADAMTS2 and COL1A1 mRNA levels. (C) PPI network prediction from the STRING database indicating a potential interaction between ADAMTS2 and COL1A1. (D, E) Validation of COL1A1 mRNA ( n =6 pairs) and protein ( n =3 pairs) levels in paired human PCa and adjacent non-tumoral tissues using qRT-PCR and WB (paired two-tailed Student’s t-test). (F, G) Reciprocal Co-IP assessments illustrating physical interaction between endogenous and exogenously expressed ADAMTS2 and COL1A1 in DU145 cells. (H) WB of COL1A1 protein levels upon ADAMTS2 overexpression or knockdown in DU145 cells. (I) Evaluation of COL1A1 upregulation and downregulation effectiveness by WB in DU145 cells. Representative images from three independent experiments are shown. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3; unpaired two-tailed Student’s t-test). *P < 0.05, ***P < 0.001.
    Figure Legend Snippet: ADAMTS2 is coexpressed and physically interacts with COL1A1 in PCa. (A) Heatmap of the top 10 genes most strongly related to ADAMTS2 expression in the TCGA-PRAD cohort. (B) Scatter plot showing the correlation between ADAMTS2 and COL1A1 mRNA levels. (C) PPI network prediction from the STRING database indicating a potential interaction between ADAMTS2 and COL1A1. (D, E) Validation of COL1A1 mRNA ( n =6 pairs) and protein ( n =3 pairs) levels in paired human PCa and adjacent non-tumoral tissues using qRT-PCR and WB (paired two-tailed Student’s t-test). (F, G) Reciprocal Co-IP assessments illustrating physical interaction between endogenous and exogenously expressed ADAMTS2 and COL1A1 in DU145 cells. (H) WB of COL1A1 protein levels upon ADAMTS2 overexpression or knockdown in DU145 cells. (I) Evaluation of COL1A1 upregulation and downregulation effectiveness by WB in DU145 cells. Representative images from three independent experiments are shown. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3; unpaired two-tailed Student’s t-test). *P < 0.05, ***P < 0.001.

    Techniques Used: Expressing, Biomarker Discovery, Quantitative RT-PCR, Two Tailed Test, Co-Immunoprecipitation Assay, Over Expression, Knockdown

    ADAMTS2 confers resistance to ferroptosis in PCa cells through COL1A1. (A) GSEA showing negative enrichment of ferroptosis-related gene signatures in TCGA-PRAD tumors with high ADAMTS2 expression. (B, C) Dose–response curves and IC 50 values for ferroptosis inducers erastin and RSL3 in control, ADAMTS2-overexpressing, and ADAMTS2-knockdown DU145 cells. IC 50 values were determined using non-linear regression analysis (n=3). (D) WB of SLC7A11 and GPX4 protein levels in ADAMTS2-knockdown cells in the presence or absence of COL1A1 overexpression. (E) WB of SLC7A11 and GPX4 in ADAMTS2-overexpressing cells in the presence or absence of COL1A1 knockdown. (F, G) MDA levels reflecting lipid peroxidation in the indicated cell groups. (H–K) Quantification of reduced GSH and oxidized GSSG under the specified genetic manipulations. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3). Statistical significance for multiple group comparisons was determined using one-way ANOVA followed by Tukey’s post hoc test. *P < 0.05.
    Figure Legend Snippet: ADAMTS2 confers resistance to ferroptosis in PCa cells through COL1A1. (A) GSEA showing negative enrichment of ferroptosis-related gene signatures in TCGA-PRAD tumors with high ADAMTS2 expression. (B, C) Dose–response curves and IC 50 values for ferroptosis inducers erastin and RSL3 in control, ADAMTS2-overexpressing, and ADAMTS2-knockdown DU145 cells. IC 50 values were determined using non-linear regression analysis (n=3). (D) WB of SLC7A11 and GPX4 protein levels in ADAMTS2-knockdown cells in the presence or absence of COL1A1 overexpression. (E) WB of SLC7A11 and GPX4 in ADAMTS2-overexpressing cells in the presence or absence of COL1A1 knockdown. (F, G) MDA levels reflecting lipid peroxidation in the indicated cell groups. (H–K) Quantification of reduced GSH and oxidized GSSG under the specified genetic manipulations. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3). Statistical significance for multiple group comparisons was determined using one-way ANOVA followed by Tukey’s post hoc test. *P < 0.05.

    Techniques Used: Expressing, Control, Knockdown, Over Expression

    Suppression of ADAMTS2 suppresses tumor growth in vivo and downregulates FAK/PI3K/AKT signaling and ferroptosis resistance markers. (A) Tumor growth curves of xenografts derived from control or ADAMTS2-knockdown DU145 cells in nude mice, evaluated every 7 days over 28 days. (n=5 mice per group). Statistical significance was determined using two-way ANOVA followed by Sidak’s multiple comparisons test. (B) Representative photographs and quantification of tumor weight at the experimental endpoint. Data are presented as the mean ± SD (n=5 mice per group; two-tailed Student’s t-test). (C) WB of ADAMTS2, p-FAK, FAK, p-PI3K, PI3K, COL1A1, p-AKT, AKT, SLC7A11, and GPX4 in excised xenograft tumor tissues. Representative blots from three independent tumor samples per group are shown. All quantitative data are presented as the mean ± SD. *P < 0.05.
    Figure Legend Snippet: Suppression of ADAMTS2 suppresses tumor growth in vivo and downregulates FAK/PI3K/AKT signaling and ferroptosis resistance markers. (A) Tumor growth curves of xenografts derived from control or ADAMTS2-knockdown DU145 cells in nude mice, evaluated every 7 days over 28 days. (n=5 mice per group). Statistical significance was determined using two-way ANOVA followed by Sidak’s multiple comparisons test. (B) Representative photographs and quantification of tumor weight at the experimental endpoint. Data are presented as the mean ± SD (n=5 mice per group; two-tailed Student’s t-test). (C) WB of ADAMTS2, p-FAK, FAK, p-PI3K, PI3K, COL1A1, p-AKT, AKT, SLC7A11, and GPX4 in excised xenograft tumor tissues. Representative blots from three independent tumor samples per group are shown. All quantitative data are presented as the mean ± SD. *P < 0.05.

    Techniques Used: In Vivo, Derivative Assay, Control, Knockdown, Two Tailed Test

    Related Articles

    Over Expression:

    Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1
    Article Snippet: .. The lentiviral particles carrying ADAMTS2 or COL1A1 overexpression constructs, as well as short hairpin RNAs (shRNAs) targeting ADAMTS2 or COL1A1, were acquired from GeneChem (China). ..

    Article Title: IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.
    Article Snippet: These cells were transfected with constructs expressing mouse Flag-IFIT3 (GeneChem, China), HA-STING, His-STING, or Flag-USP18 (YouBio, China) using Lipofectamine 2000 (Invitrogen, USA) according to the manufacturer’s instructions. .. For lentiviral infection, cells were transduced with lentiviruses carrying IFIT3 shRNA or overexpression constructs (GeneChem, China) at a multiplicity of infection (MOI) of 50. ..

    Article Title: YARS2 mediates PARPi resistance in pancreatic cancer by regulating the MYC-E2F axis.
    Article Snippet: Background: Pancreatic ductal adenocarcinoma (PDAC) resistance to PARP inhibitors (PARPi) remains poorly understood, the mechanism of resistance remain poorly understood.. Material and Methods: We integrated multi-omics data from The Cancer Genome Atlas-Pancreatic Adenocarcinoma (TCGA-PAAD) datasets, Cancer Cell Line Encyclopedia (CCLE), and the Genomics of Drug Sensitivity in Cancer (GDSC) performed weighted gene co-expression network analysis (WGCNA) to identify hub genes linked to PARPi resistance.. GSE86394 from the Gene Expression Omnibus (GEO) database was utilized to differential expressed genes (DEGs) and performed functional enrichment analyses.

    Article Title: LDHC4 promotes ovarian cancer progression through H4K12 lactylation to regulate PGK1 expression and modulate glycolysis
    Article Snippet: .. The experimental design included overexpression constructs (LDHC4-OE and Mock; supplied by Genechem, Shanghai) and shRNA knockdown groups (si-LDHC4 and si-NC; also from Genechem), each set up with 3 to 5 replicate wells. .. After incubation at 37 °C under 5% CO2 for 0, 24, 48, 72, or 96 h, 10 μL of CCK-8 reagent (Beyotime, Shanghai, China) was added to each well, followed by further incubation for 3 h. Absorbance was measured at 450 nm and 630 nm using a Multiskan spectrophotometer (Thermo, USA).

    Article Title: Mitochondrial complex I subunit NDUFS4 overexpression drives glioma progression by regulating mitochondrial function and COX5B.
    Article Snippet: Antibodies were sourced from Cellular Signaling Tech (Danvers, MA) and Abcam (Cambridge, United Kingdom). .. Genechem (Shanghai, China) provided the validated mRNA primers, as well as shRNA, knockout and overexpression viral constructs. .. Serum, AR TI CL E IN P RE SS FBS, high-glucose medium, and antibiotics were supplied by Hyclone (Logan, UT).

    Article Title: SAPCD2 Drives Bladder Cancer Progression by Stabilizing TANK and Engaging a CREB–PLAGL2 Feedback Loop to Sustain MAPK Signaling
    Article Snippet: .. Lentiviruses carrying PLAGL2 or TANK overexpression constructs, as well as lentiviruses encoding specific shRNAs targeting PLAGL2 or TANK, were designed and packaged by GeneChem (Shanghai, China). ..

    Article Title: SAPCD2 Drives Bladder Cancer Progression by Stabilizing TANK and Engaging a CREB-PLAGL2 Feedback Loop to Sustain MAPK Signaling.
    Article Snippet: .. Lentiviruses carrying PLAGL2 or TANK overexpression constructs, as well as lentiviruses encoding specific shRNAs targeting PLAGL2 or TANK, were designed and packaged by GeneChem (Shanghai, China). ..

    Construct:

    Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1
    Article Snippet: .. The lentiviral particles carrying ADAMTS2 or COL1A1 overexpression constructs, as well as short hairpin RNAs (shRNAs) targeting ADAMTS2 or COL1A1, were acquired from GeneChem (China). ..

    Article Title: IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.
    Article Snippet: These cells were transfected with constructs expressing mouse Flag-IFIT3 (GeneChem, China), HA-STING, His-STING, or Flag-USP18 (YouBio, China) using Lipofectamine 2000 (Invitrogen, USA) according to the manufacturer’s instructions. .. For lentiviral infection, cells were transduced with lentiviruses carrying IFIT3 shRNA or overexpression constructs (GeneChem, China) at a multiplicity of infection (MOI) of 50. ..

    Article Title: YARS2 mediates PARPi resistance in pancreatic cancer by regulating the MYC-E2F axis.
    Article Snippet: Background: Pancreatic ductal adenocarcinoma (PDAC) resistance to PARP inhibitors (PARPi) remains poorly understood, the mechanism of resistance remain poorly understood.. Material and Methods: We integrated multi-omics data from The Cancer Genome Atlas-Pancreatic Adenocarcinoma (TCGA-PAAD) datasets, Cancer Cell Line Encyclopedia (CCLE), and the Genomics of Drug Sensitivity in Cancer (GDSC) performed weighted gene co-expression network analysis (WGCNA) to identify hub genes linked to PARPi resistance.. GSE86394 from the Gene Expression Omnibus (GEO) database was utilized to differential expressed genes (DEGs) and performed functional enrichment analyses.

    Article Title: LDHC4 promotes ovarian cancer progression through H4K12 lactylation to regulate PGK1 expression and modulate glycolysis
    Article Snippet: .. The experimental design included overexpression constructs (LDHC4-OE and Mock; supplied by Genechem, Shanghai) and shRNA knockdown groups (si-LDHC4 and si-NC; also from Genechem), each set up with 3 to 5 replicate wells. .. After incubation at 37 °C under 5% CO2 for 0, 24, 48, 72, or 96 h, 10 μL of CCK-8 reagent (Beyotime, Shanghai, China) was added to each well, followed by further incubation for 3 h. Absorbance was measured at 450 nm and 630 nm using a Multiskan spectrophotometer (Thermo, USA).

    Article Title: Mitochondrial complex I subunit NDUFS4 overexpression drives glioma progression by regulating mitochondrial function and COX5B.
    Article Snippet: Antibodies were sourced from Cellular Signaling Tech (Danvers, MA) and Abcam (Cambridge, United Kingdom). .. Genechem (Shanghai, China) provided the validated mRNA primers, as well as shRNA, knockout and overexpression viral constructs. .. Serum, AR TI CL E IN P RE SS FBS, high-glucose medium, and antibiotics were supplied by Hyclone (Logan, UT).

    Article Title: SAPCD2 Drives Bladder Cancer Progression by Stabilizing TANK and Engaging a CREB–PLAGL2 Feedback Loop to Sustain MAPK Signaling
    Article Snippet: .. Lentiviruses carrying PLAGL2 or TANK overexpression constructs, as well as lentiviruses encoding specific shRNAs targeting PLAGL2 or TANK, were designed and packaged by GeneChem (Shanghai, China). ..

    Article Title: SAPCD2 Drives Bladder Cancer Progression by Stabilizing TANK and Engaging a CREB-PLAGL2 Feedback Loop to Sustain MAPK Signaling.
    Article Snippet: .. Lentiviruses carrying PLAGL2 or TANK overexpression constructs, as well as lentiviruses encoding specific shRNAs targeting PLAGL2 or TANK, were designed and packaged by GeneChem (Shanghai, China). ..

    Infection:

    Article Title: IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.
    Article Snippet: These cells were transfected with constructs expressing mouse Flag-IFIT3 (GeneChem, China), HA-STING, His-STING, or Flag-USP18 (YouBio, China) using Lipofectamine 2000 (Invitrogen, USA) according to the manufacturer’s instructions. .. For lentiviral infection, cells were transduced with lentiviruses carrying IFIT3 shRNA or overexpression constructs (GeneChem, China) at a multiplicity of infection (MOI) of 50. ..

    Transduction:

    Article Title: IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.
    Article Snippet: These cells were transfected with constructs expressing mouse Flag-IFIT3 (GeneChem, China), HA-STING, His-STING, or Flag-USP18 (YouBio, China) using Lipofectamine 2000 (Invitrogen, USA) according to the manufacturer’s instructions. .. For lentiviral infection, cells were transduced with lentiviruses carrying IFIT3 shRNA or overexpression constructs (GeneChem, China) at a multiplicity of infection (MOI) of 50. ..

    shRNA:

    Article Title: IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.
    Article Snippet: These cells were transfected with constructs expressing mouse Flag-IFIT3 (GeneChem, China), HA-STING, His-STING, or Flag-USP18 (YouBio, China) using Lipofectamine 2000 (Invitrogen, USA) according to the manufacturer’s instructions. .. For lentiviral infection, cells were transduced with lentiviruses carrying IFIT3 shRNA or overexpression constructs (GeneChem, China) at a multiplicity of infection (MOI) of 50. ..

    Article Title: LDHC4 promotes ovarian cancer progression through H4K12 lactylation to regulate PGK1 expression and modulate glycolysis
    Article Snippet: .. The experimental design included overexpression constructs (LDHC4-OE and Mock; supplied by Genechem, Shanghai) and shRNA knockdown groups (si-LDHC4 and si-NC; also from Genechem), each set up with 3 to 5 replicate wells. .. After incubation at 37 °C under 5% CO2 for 0, 24, 48, 72, or 96 h, 10 μL of CCK-8 reagent (Beyotime, Shanghai, China) was added to each well, followed by further incubation for 3 h. Absorbance was measured at 450 nm and 630 nm using a Multiskan spectrophotometer (Thermo, USA).

    Article Title: Mitochondrial complex I subunit NDUFS4 overexpression drives glioma progression by regulating mitochondrial function and COX5B.
    Article Snippet: Antibodies were sourced from Cellular Signaling Tech (Danvers, MA) and Abcam (Cambridge, United Kingdom). .. Genechem (Shanghai, China) provided the validated mRNA primers, as well as shRNA, knockout and overexpression viral constructs. .. Serum, AR TI CL E IN P RE SS FBS, high-glucose medium, and antibiotics were supplied by Hyclone (Logan, UT).

    Negative Control:

    Article Title: YARS2 mediates PARPi resistance in pancreatic cancer by regulating the MYC-E2F axis.
    Article Snippet: Background: Pancreatic ductal adenocarcinoma (PDAC) resistance to PARP inhibitors (PARPi) remains poorly understood, the mechanism of resistance remain poorly understood.. Material and Methods: We integrated multi-omics data from The Cancer Genome Atlas-Pancreatic Adenocarcinoma (TCGA-PAAD) datasets, Cancer Cell Line Encyclopedia (CCLE), and the Genomics of Drug Sensitivity in Cancer (GDSC) performed weighted gene co-expression network analysis (WGCNA) to identify hub genes linked to PARPi resistance.. GSE86394 from the Gene Expression Omnibus (GEO) database was utilized to differential expressed genes (DEGs) and performed functional enrichment analyses.

    Synthesized:

    Article Title: YARS2 mediates PARPi resistance in pancreatic cancer by regulating the MYC-E2F axis.
    Article Snippet: Background: Pancreatic ductal adenocarcinoma (PDAC) resistance to PARP inhibitors (PARPi) remains poorly understood, the mechanism of resistance remain poorly understood.. Material and Methods: We integrated multi-omics data from The Cancer Genome Atlas-Pancreatic Adenocarcinoma (TCGA-PAAD) datasets, Cancer Cell Line Encyclopedia (CCLE), and the Genomics of Drug Sensitivity in Cancer (GDSC) performed weighted gene co-expression network analysis (WGCNA) to identify hub genes linked to PARPi resistance.. GSE86394 from the Gene Expression Omnibus (GEO) database was utilized to differential expressed genes (DEGs) and performed functional enrichment analyses.

    Knockdown:

    Article Title: LDHC4 promotes ovarian cancer progression through H4K12 lactylation to regulate PGK1 expression and modulate glycolysis
    Article Snippet: .. The experimental design included overexpression constructs (LDHC4-OE and Mock; supplied by Genechem, Shanghai) and shRNA knockdown groups (si-LDHC4 and si-NC; also from Genechem), each set up with 3 to 5 replicate wells. .. After incubation at 37 °C under 5% CO2 for 0, 24, 48, 72, or 96 h, 10 μL of CCK-8 reagent (Beyotime, Shanghai, China) was added to each well, followed by further incubation for 3 h. Absorbance was measured at 450 nm and 630 nm using a Multiskan spectrophotometer (Thermo, USA).

    Knock-Out:

    Article Title: Mitochondrial complex I subunit NDUFS4 overexpression drives glioma progression by regulating mitochondrial function and COX5B.
    Article Snippet: Antibodies were sourced from Cellular Signaling Tech (Danvers, MA) and Abcam (Cambridge, United Kingdom). .. Genechem (Shanghai, China) provided the validated mRNA primers, as well as shRNA, knockout and overexpression viral constructs. .. Serum, AR TI CL E IN P RE SS FBS, high-glucose medium, and antibiotics were supplied by Hyclone (Logan, UT).



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    Significantly differentially expressed ECM molecules in early, mid and late-stage mammary tumor samples from the PyMT mouse model of breast cancer in comparison to healthy fat pad tissue (A) PCA of individual samples ( n = 4 or 5 mice per group). Principal components 1 and 2 account for 81.6% of the variability in the dataset. (B) Heatmap of significantly differentially deposited matrisomal elements between groups within the dataset (left). Missing values are shaded in gray. Four major clusters were identified based on Euclidian hierarchical clustering of proteins (middle) and the matrisome categorical annotation for these clustered matrisomal elements based on the matrisome project is shown (right). Expression of <t>PXDN</t> in each sample (cluster 3) is highlighted in red.
    Stable Cell Line Generation Lentiviral Shrna Constructs Targeting Cfb Sh Cfb, supplied by Ubigene Biosciences Co Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    short hairpin rna shrna constructs  (Genechem)
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    Genechem short hairpin rna shrna constructs
    Significantly differentially expressed ECM molecules in early, mid and late-stage mammary tumor samples from the PyMT mouse model of breast cancer in comparison to healthy fat pad tissue (A) PCA of individual samples ( n = 4 or 5 mice per group). Principal components 1 and 2 account for 81.6% of the variability in the dataset. (B) Heatmap of significantly differentially deposited matrisomal elements between groups within the dataset (left). Missing values are shaded in gray. Four major clusters were identified based on Euclidian hierarchical clustering of proteins (middle) and the matrisome categorical annotation for these clustered matrisomal elements based on the matrisome project is shown (right). Expression of <t>PXDN</t> in each sample (cluster 3) is highlighted in red.
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    lentiviral shrna constructs targeting shp  (OriGene)
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    OriGene lentiviral shrna constructs targeting shp
    ( A ) <t>Relative</t> <t>SHP-1</t> protein expression in the 19 BCa cell lines examined in this study. ( B ) Expression levels were significantly higher in epithelial-like cells (n = 11) than in intermediate and mesenchymal-like lines (n = 8). Error bars represent the standard error of the mean (SEM).
    Lentiviral Shrna Constructs Targeting Shp, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Significantly differentially expressed ECM molecules in early, mid and late-stage mammary tumor samples from the PyMT mouse model of breast cancer in comparison to healthy fat pad tissue (A) PCA of individual samples ( n = 4 or 5 mice per group). Principal components 1 and 2 account for 81.6% of the variability in the dataset. (B) Heatmap of significantly differentially deposited matrisomal elements between groups within the dataset (left). Missing values are shaded in gray. Four major clusters were identified based on Euclidian hierarchical clustering of proteins (middle) and the matrisome categorical annotation for these clustered matrisomal elements based on the matrisome project is shown (right). Expression of PXDN in each sample (cluster 3) is highlighted in red.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: Significantly differentially expressed ECM molecules in early, mid and late-stage mammary tumor samples from the PyMT mouse model of breast cancer in comparison to healthy fat pad tissue (A) PCA of individual samples ( n = 4 or 5 mice per group). Principal components 1 and 2 account for 81.6% of the variability in the dataset. (B) Heatmap of significantly differentially deposited matrisomal elements between groups within the dataset (left). Missing values are shaded in gray. Four major clusters were identified based on Euclidian hierarchical clustering of proteins (middle) and the matrisome categorical annotation for these clustered matrisomal elements based on the matrisome project is shown (right). Expression of PXDN in each sample (cluster 3) is highlighted in red.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: Comparison, Expressing

    Association of PXDN expression with patient overall survival Significance between Kaplan-Meier survival curves were calculated with the log-rank test. (A) Overall survival of 1,082 patients from the TCGA breast cancer cohort stratified by median mRNA expression of PXDN. (B) Overall survival of 1,082 patients from the TCGA breast cancer cohort separated by disease stage, and stratified by median mRNA expression of PXDN (dotted line = low PXDN expression, solid line = high PXDN expression) and stage of disease (stage I, red; II, gold; III, green; IV, blue; or unknown, purple). (C) Extraction of data from (B) showing patients with stage II breast cancer at the time of diagnosis stratified by median mRNA expression of PXDN (dotted line = low PXDN expression, solid line = high PXDN expression) ( n = 615). (D) Examples of PXDN IHC staining intensity and corresponding intensity scores for the stromal and epithelial compartments of tumors ( n = 334). Scale bars, 50 μm. (E) Overall survival of 311 invasive ductal carcinoma patients from the CREA tumor microarray cohort stratified by high vs. low Allred-scores for PXDN IHC staining of epithelial compartments of tumors. (F) Overall survival of 309 invasive ductal carcinoma patients from the CREA tumor microarray cohort stratified by high vs. low Allred-scores for PXDN IHC staining of stromal compartments of tumors. (G) Overall survival of invasive ductal carcinoma patients from the CREA tumor microarray cohort stratified by combined stromal and epithelial Allred-scores for PXDN IHC staining of cores. Log-rank p values between each curve of (G) are listed in .

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: Association of PXDN expression with patient overall survival Significance between Kaplan-Meier survival curves were calculated with the log-rank test. (A) Overall survival of 1,082 patients from the TCGA breast cancer cohort stratified by median mRNA expression of PXDN. (B) Overall survival of 1,082 patients from the TCGA breast cancer cohort separated by disease stage, and stratified by median mRNA expression of PXDN (dotted line = low PXDN expression, solid line = high PXDN expression) and stage of disease (stage I, red; II, gold; III, green; IV, blue; or unknown, purple). (C) Extraction of data from (B) showing patients with stage II breast cancer at the time of diagnosis stratified by median mRNA expression of PXDN (dotted line = low PXDN expression, solid line = high PXDN expression) ( n = 615). (D) Examples of PXDN IHC staining intensity and corresponding intensity scores for the stromal and epithelial compartments of tumors ( n = 334). Scale bars, 50 μm. (E) Overall survival of 311 invasive ductal carcinoma patients from the CREA tumor microarray cohort stratified by high vs. low Allred-scores for PXDN IHC staining of epithelial compartments of tumors. (F) Overall survival of 309 invasive ductal carcinoma patients from the CREA tumor microarray cohort stratified by high vs. low Allred-scores for PXDN IHC staining of stromal compartments of tumors. (G) Overall survival of invasive ductal carcinoma patients from the CREA tumor microarray cohort stratified by combined stromal and epithelial Allred-scores for PXDN IHC staining of cores. Log-rank p values between each curve of (G) are listed in .

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: Expressing, Extraction, Biomarker Discovery, Immunohistochemistry, Microarray

    Single cell analysis of breast tumor cells expressing PXDN (A–C) Murine PyMT tumor single cell data (11,490 cells) obtained from Valdés-Mora et al. (A) UMAP of the major cell types identified in the murine single cell data. (B) UMAP of PXDN expression across cells. (C) Violin plots of fold change in PXDN expression according to cell type in the murine dataset. (D and E) Human breast cancer single cell and spatial data containing 130,246 cells from 26 invasive breast cancer patients. (D) UMAP of the major cell types identified in the human single cell data. (E) UMAP of PXDN expression across human cells. (F) Boxplots of fold change in PXDN expression according to cell type in the human dataset.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: Single cell analysis of breast tumor cells expressing PXDN (A–C) Murine PyMT tumor single cell data (11,490 cells) obtained from Valdés-Mora et al. (A) UMAP of the major cell types identified in the murine single cell data. (B) UMAP of PXDN expression across cells. (C) Violin plots of fold change in PXDN expression according to cell type in the murine dataset. (D and E) Human breast cancer single cell and spatial data containing 130,246 cells from 26 invasive breast cancer patients. (D) UMAP of the major cell types identified in the human single cell data. (E) UMAP of PXDN expression across human cells. (F) Boxplots of fold change in PXDN expression according to cell type in the human dataset.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: Single-cell Analysis, Expressing, Single Cell

    PXDN affects cell proliferation and spheroid formation dynamics in CAFs Differences between shScr CAFs and sh#1 CAFs, or between WT CAFs and OE CAFs, were calculated using Student’s t tests and p values are shown on each graph. p values <0.05 were considered significant. ns = not significant. (A and C) RNA expression of PXDN in shScr and sh#1 (A), or WT and OE (C) CAFs. Error bars show the standard deviation of six independent experiments. (B and D) Representative western blots showing PXDN levels in conditioned media (top) from shScr and sh#1 CAFs (B) or WT and OE CAFs (D), with densitometry quantification of three biological replicate western blots (bottom). Densitometry measurements were normalized to total protein loading (measured by Ponceau S stain) and calculated relative to control (shScr or WT) protein expression. (E and F) 2D proliferation of shScr and sh#1 CAFs (E) or WT and OE CAFs (F) as measured by Alamar blue assay five days of culture (left). Differences between CAF lines were directly compared on day 5 (right). Error bars indicate the standard error of the mean for three biological replicates. (G–L) 3D growth of shScr (blue), sh#1 (red), WT (purple), and OE (gold) CAFs as spheroids over the course of 16 days. (G and I) Spheroid area and (K and L) representative images over the course of 16 days. Scale bars, 400 μm. Dotted lines indicate media changes on days 4, 8, and 12. Error bars indicate the standard error of the mean for three biological replicates. (H and J) The day of spheroid growth at which spheroids reached their smallest size before expanding. Error bars indicate the standard error of 24 spheroids across three biological replicates.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: PXDN affects cell proliferation and spheroid formation dynamics in CAFs Differences between shScr CAFs and sh#1 CAFs, or between WT CAFs and OE CAFs, were calculated using Student’s t tests and p values are shown on each graph. p values <0.05 were considered significant. ns = not significant. (A and C) RNA expression of PXDN in shScr and sh#1 (A), or WT and OE (C) CAFs. Error bars show the standard deviation of six independent experiments. (B and D) Representative western blots showing PXDN levels in conditioned media (top) from shScr and sh#1 CAFs (B) or WT and OE CAFs (D), with densitometry quantification of three biological replicate western blots (bottom). Densitometry measurements were normalized to total protein loading (measured by Ponceau S stain) and calculated relative to control (shScr or WT) protein expression. (E and F) 2D proliferation of shScr and sh#1 CAFs (E) or WT and OE CAFs (F) as measured by Alamar blue assay five days of culture (left). Differences between CAF lines were directly compared on day 5 (right). Error bars indicate the standard error of the mean for three biological replicates. (G–L) 3D growth of shScr (blue), sh#1 (red), WT (purple), and OE (gold) CAFs as spheroids over the course of 16 days. (G and I) Spheroid area and (K and L) representative images over the course of 16 days. Scale bars, 400 μm. Dotted lines indicate media changes on days 4, 8, and 12. Error bars indicate the standard error of the mean for three biological replicates. (H and J) The day of spheroid growth at which spheroids reached their smallest size before expanding. Error bars indicate the standard error of 24 spheroids across three biological replicates.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: RNA Expression, Standard Deviation, Western Blot, Staining, Control, Expressing, Alamar Blue Assay

    PXDN inhibits the ability of CAFs to remodel collagen matrices (A and C) Representative images of collagen matrices contraction over the course of 12 days when seeded with shScr or sh#1 CAFs (A) or WT or OE CAFs (C). Scale bars, 1 cm. (B and D) Area of matrices during contraction over the course of 12 days (left), with differences in final area of matrices compared at day 12 (right). Error bars indicate the standard error of the mean for three biological replicates. p values were calculated using Student’s t tests. p values <0.05 were considered significant.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: PXDN inhibits the ability of CAFs to remodel collagen matrices (A and C) Representative images of collagen matrices contraction over the course of 12 days when seeded with shScr or sh#1 CAFs (A) or WT or OE CAFs (C). Scale bars, 1 cm. (B and D) Area of matrices during contraction over the course of 12 days (left), with differences in final area of matrices compared at day 12 (right). Error bars indicate the standard error of the mean for three biological replicates. p values were calculated using Student’s t tests. p values <0.05 were considered significant.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques:

    Impact of CAF-produced PXDN on cancer cell proliferation and motility Differences between shScr CAFs and sh#1 CAFs, or between WT CAFs and OE CAFs, were calculated using Student’s t tests and p values are indicated on each graph. p values <0.05 were considered significant. ns = not significant. (A) Schematic of generation of CAF-generated CDMs, onto which cancer cells were seeded. (B and C) Proliferation rates of cancer cells seeded on CDMs produced by sh#1 or shScr CAFs (B), or by WT and OE CAFs (C) as measured by Alamar blue at day 7. Error bars represent the standard deviation of eight replicates. (D and F) Mean velocity of cancer cells when seeded onto CDMs produced by shScr or sh#1 CAFs (D) or by WT or OE CAFs (F). (E and G) Distance traveled by cancer cells when seeded onto CDMs produced by shScr or sh#1 CAFs (E) or by WT or OE CAFs (G). A minimum of ten cells were tracked per biological replicate, across three biological replicates. Error bars indicate the standard deviation.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: Impact of CAF-produced PXDN on cancer cell proliferation and motility Differences between shScr CAFs and sh#1 CAFs, or between WT CAFs and OE CAFs, were calculated using Student’s t tests and p values are indicated on each graph. p values <0.05 were considered significant. ns = not significant. (A) Schematic of generation of CAF-generated CDMs, onto which cancer cells were seeded. (B and C) Proliferation rates of cancer cells seeded on CDMs produced by sh#1 or shScr CAFs (B), or by WT and OE CAFs (C) as measured by Alamar blue at day 7. Error bars represent the standard deviation of eight replicates. (D and F) Mean velocity of cancer cells when seeded onto CDMs produced by shScr or sh#1 CAFs (D) or by WT or OE CAFs (F). (E and G) Distance traveled by cancer cells when seeded onto CDMs produced by shScr or sh#1 CAFs (E) or by WT or OE CAFs (G). A minimum of ten cells were tracked per biological replicate, across three biological replicates. Error bars indicate the standard deviation.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: Produced, Generated, Standard Deviation

    Effect of CAF PXDN expression on breast tumor progression in vivo Differences between shScr CAFs and sh#1 CAFs, or between WT CAFs and OE CAFs, were calculated using Student’s t tests and p values are indicated on each graph. p values <0.05 were considered significant; ns = not significant. (A and B) Latency of tumor formation from the time cells were implanted into mice along with shScr or sh#1 CAFs (A) or with WT or OE CAFs (B) until tumors reached 50 mm 3 in size. (C and D) Final weights of tumors upon collection from mice implanted with cancer cells and shScr or sh#1 CAFs (C) or with WT or OE CAFs (D). (E) Representative images of α-SMA staining in tumors from shScr or sh#1 CAF tumors. Scale bars, 100 μm. (F) Quantification of α-SMA staining in shScr and sh#1 CAF tumors. Error bars indicate the standard deviation. (G) Representative images of α-SMA staining in tumors from WT or OE CAF tumors. Scale bars, 100 μm. (H) Quantification of α-SMA staining in WT and OE CAF tumors. Error bars indicate the standard deviation.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: Effect of CAF PXDN expression on breast tumor progression in vivo Differences between shScr CAFs and sh#1 CAFs, or between WT CAFs and OE CAFs, were calculated using Student’s t tests and p values are indicated on each graph. p values <0.05 were considered significant; ns = not significant. (A and B) Latency of tumor formation from the time cells were implanted into mice along with shScr or sh#1 CAFs (A) or with WT or OE CAFs (B) until tumors reached 50 mm 3 in size. (C and D) Final weights of tumors upon collection from mice implanted with cancer cells and shScr or sh#1 CAFs (C) or with WT or OE CAFs (D). (E) Representative images of α-SMA staining in tumors from shScr or sh#1 CAF tumors. Scale bars, 100 μm. (F) Quantification of α-SMA staining in shScr and sh#1 CAF tumors. Error bars indicate the standard deviation. (G) Representative images of α-SMA staining in tumors from WT or OE CAF tumors. Scale bars, 100 μm. (H) Quantification of α-SMA staining in WT and OE CAF tumors. Error bars indicate the standard deviation.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: Expressing, In Vivo, Staining, Standard Deviation

    Effect of PXDN inhibition on breast tumor progression using AZD5904 (A) Inhibition of PXDN by a range of concentrations of AZD5904 measured on live cells using a modified Amplex red activity assay. Resorufin fluorescence was monitored continuously for 1 h. Error bars indicate standard error of the mean across three biological replicates, each consisting of eight technical replicates. (B) Final resorufin fluorescence readings at 60 min were used to determine to IC50 inhibitory concentration of AZD5904. (C) Kaplan-Meier curve of mouse survival measured from the start of treatment with AZD5904 or vehicle (when tumors reached a detectable size of 50 mm 3 ) until tumors reached a maximum ethical size of 1 cm by 1 cm and mice were sacrificed. Survival curves were significantly different, with a log-rank p value of 0.0088. (D) Final weights of tumors upon collection from mice in the AZD5904 in vivo study. Error bars indicate the standard deviation. Student’s t test showed no statistical significance between vehicle and AZD5904 treatment groups. (E) Time taken for tumors to reach the detectable size of 50 mm 3 at which point treatment started. Error bars indicate the standard deviation. Student’s t test showed no statistical significance between vehicle and AZD5904 treatment groups.

    Journal: iScience

    Article Title: Stromal peroxidasin drives early tumor growth in breast cancer

    doi: 10.1016/j.isci.2026.116078

    Figure Lengend Snippet: Effect of PXDN inhibition on breast tumor progression using AZD5904 (A) Inhibition of PXDN by a range of concentrations of AZD5904 measured on live cells using a modified Amplex red activity assay. Resorufin fluorescence was monitored continuously for 1 h. Error bars indicate standard error of the mean across three biological replicates, each consisting of eight technical replicates. (B) Final resorufin fluorescence readings at 60 min were used to determine to IC50 inhibitory concentration of AZD5904. (C) Kaplan-Meier curve of mouse survival measured from the start of treatment with AZD5904 or vehicle (when tumors reached a detectable size of 50 mm 3 ) until tumors reached a maximum ethical size of 1 cm by 1 cm and mice were sacrificed. Survival curves were significantly different, with a log-rank p value of 0.0088. (D) Final weights of tumors upon collection from mice in the AZD5904 in vivo study. Error bars indicate the standard deviation. Student’s t test showed no statistical significance between vehicle and AZD5904 treatment groups. (E) Time taken for tumors to reach the detectable size of 50 mm 3 at which point treatment started. Error bars indicate the standard deviation. Student’s t test showed no statistical significance between vehicle and AZD5904 treatment groups.

    Article Snippet: Lentiviral PXDN shRNA knockdown constructs and a Scrambled control construct containing GFP sequences were obtained from OriGene (TL513178V).

    Techniques: Inhibition, Modification, Activity Assay, Fluorescence, Concentration Assay, In Vivo, Standard Deviation

    ( A ) Relative SHP-1 protein expression in the 19 BCa cell lines examined in this study. ( B ) Expression levels were significantly higher in epithelial-like cells (n = 11) than in intermediate and mesenchymal-like lines (n = 8). Error bars represent the standard error of the mean (SEM).

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: ( A ) Relative SHP-1 protein expression in the 19 BCa cell lines examined in this study. ( B ) Expression levels were significantly higher in epithelial-like cells (n = 11) than in intermediate and mesenchymal-like lines (n = 8). Error bars represent the standard error of the mean (SEM).

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Expressing

    ( A ) SHP-1 protein expression in bladder tissue was significantly lower in muscle-invasive (MI, n = 8) tumor than in non-muscle-invasive (NMI, n = 8) and urothelial tissue with no residual disease (NRD, n = 10). ( B ) Examples of DAB and corresponding H&E staining in the bladder tissues examined in this study. The error bars represent the interquartile range.

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: ( A ) SHP-1 protein expression in bladder tissue was significantly lower in muscle-invasive (MI, n = 8) tumor than in non-muscle-invasive (NMI, n = 8) and urothelial tissue with no residual disease (NRD, n = 10). ( B ) Examples of DAB and corresponding H&E staining in the bladder tissues examined in this study. The error bars represent the interquartile range.

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Expressing, Staining

    Correlation plots (n = 19) of SHP-1 protein expression with the EMT markers E-cadherin, N-cadherin, and Vimentin. Gray areas represent the 95%CI. Representative Western blot images: from the BCa cell lines EJ and HT-1376, the first lane of each pair corresponds to the protein indicated above each lane, and the second corresponds to the total protein detected for the same lane.

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: Correlation plots (n = 19) of SHP-1 protein expression with the EMT markers E-cadherin, N-cadherin, and Vimentin. Gray areas represent the 95%CI. Representative Western blot images: from the BCa cell lines EJ and HT-1376, the first lane of each pair corresponds to the protein indicated above each lane, and the second corresponds to the total protein detected for the same lane.

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Expressing, Western Blot

    ( A ) SHP-1 protein expression following transduction with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 6, RT-112 n = 7, TCCSUP n = 4, UM-UC-3 n = 6. ( B ) Representative Western blot images: the first lane of each pair corresponds to SHP-1, and the second corresponds to the total protein detected for the same lane. Error bars represent the SEM. ( C ) Relative proliferation rates of BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 5, RT-112 n = 5, TCCSUP n = 9, UM-UC-3 n = 5. Error bars represent the SEM.

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: ( A ) SHP-1 protein expression following transduction with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 6, RT-112 n = 7, TCCSUP n = 4, UM-UC-3 n = 6. ( B ) Representative Western blot images: the first lane of each pair corresponds to SHP-1, and the second corresponds to the total protein detected for the same lane. Error bars represent the SEM. ( C ) Relative proliferation rates of BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 5, RT-112 n = 5, TCCSUP n = 9, UM-UC-3 n = 5. Error bars represent the SEM.

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Expressing, Transduction, shRNA, Western Blot

    ( A ) Relative migration rates of BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 5, RT-112 n = 4, TCCSUP n = 3, UM-UC-3 n = 3. ( B ) Representative images from in vitro migration assays (scale bar = 200 μm). ( C ) Relative invasion rates of BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 3, RT-112 n = 5, TCCSUP n = 3, UM-UC-3 n = 3. ( D ) Representative images from in vitro invasion assays (scale bar = 200 μm). Error bars represent the SEM.

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: ( A ) Relative migration rates of BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 5, RT-112 n = 4, TCCSUP n = 3, UM-UC-3 n = 3. ( B ) Representative images from in vitro migration assays (scale bar = 200 μm). ( C ) Relative invasion rates of BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): CUBIII n = 3, RT-112 n = 5, TCCSUP n = 3, UM-UC-3 n = 3. ( D ) Representative images from in vitro invasion assays (scale bar = 200 μm). Error bars represent the SEM.

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Migration, Transduction, shRNA, In Vitro

    Significant gene sets resulting from GSEA of RNA sequence data comparing the transduced BCa lines with high-SHP-1-expressing lines versus low-SHP-1-expressing lines (q-value < 0.1).

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: Significant gene sets resulting from GSEA of RNA sequence data comparing the transduced BCa lines with high-SHP-1-expressing lines versus low-SHP-1-expressing lines (q-value < 0.1).

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Sequencing, Expressing

    Relative expression of pAkt/Akt in BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): RT-112 n = 7 and TCCSUP n = 8. Representative Western blot images: the first lane of each pair corresponds to Akt or pAkt (ser473), and the second corresponds to the total protein detected for the same lane. Error bars represent the SEM.

    Journal: Cancers

    Article Title: Evidence for a Tumor-Suppressive Role of SHP-1 in EMT Regulation in Bladder Cancer Cells

    doi: 10.3390/cancers18091401

    Figure Lengend Snippet: Relative expression of pAkt/Akt in BCa cells transduced with SHP-1 shRNA (shSHP-1) or SHP-1 cDNA (+SHP-1) and corresponding negative controls (NC): RT-112 n = 7 and TCCSUP n = 8. Representative Western blot images: the first lane of each pair corresponds to Akt or pAkt (ser473), and the second corresponds to the total protein detected for the same lane. Error bars represent the SEM.

    Article Snippet: Lentiviral shRNA constructs targeting SHP-1 were obtained from Origene (Rockville, MD, USA), and the manufacturer’s protocol was used to establish stable cell lines for each construct.

    Techniques: Expressing, Transduction, shRNA, Western Blot