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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/result/col1a1 overexpression constructs/product/Genechem
    Average 86 stars, based on 1 article reviews
    col1a1 overexpression constructs - by Bioz Stars, 2026-06
    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



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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/result/col1a1 overexpression constructs/product/Genechem
    Average 86 stars, based on 1 article reviews
    col1a1 overexpression constructs - by Bioz Stars, 2026-06
    86/100 stars
    		  Buy from Supplier

    Image Search Results


    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.

    Journal: Frontiers in Oncology

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

    doi: 10.3389/fonc.2026.1784882

    Figure Lengend 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.

    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).

    Techniques: 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.

    Journal: Frontiers in Oncology

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

    doi: 10.3389/fonc.2026.1784882

    Figure Lengend 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.

    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).

    Techniques: 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.

    Journal: Frontiers in Oncology

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

    doi: 10.3389/fonc.2026.1784882

    Figure Lengend 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.

    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).

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