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human prostate cancer cell line du 145  (ATCC)


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    Structured Review

    ATCC human prostate cancer cell line du 145
    Human Prostate Cancer Cell Line Du 145, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 9831 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human prostate cancer cell line du 145/product/ATCC
    Average 99 stars, based on 9831 article reviews
    human prostate cancer cell line du 145 - by Bioz Stars, 2026-02
    99/100 stars

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    ATCC du145 human prostate cancer cell line
    GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in <t>DU145</t> cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
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    ATCC human prostate cancer cell line du145
    GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in <t>DU145</t> cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
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    https://www.bioz.com/result/human prostate cancer cell line du145/product/ATCC
    Average 99 stars, based on 1 article reviews
    human prostate cancer cell line du145 - by Bioz Stars, 2026-02
    99/100 stars
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    GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in <t>DU145</t> cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
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    GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in DU145 cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Journal: Frontiers in Immunology

    Article Title: Identify GDPD3 as a key regulator of epithelial–mesenchymal transition and prostate adenocarcinoma progression via the LPA/LPAR1/AKT axis: transcriptomic and experimental study

    doi: 10.3389/fimmu.2025.1637325

    Figure Lengend Snippet: GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in DU145 cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: The DU145 human prostate cancer cell line was obtained from the American Type Culture Collection (ATCC) in February 2025.

    Techniques: Enzyme-linked Immunosorbent Assay, Over Expression, Control, Western Blot, Software

    LPAR1 knockdown and AKT inhibition attenuate LPA-induced EMT. (A, B) LPAR1 was knocked down, and knockdown efficiency was subsequently validated. (C, D) DU145 cells were transfected with siRNA targeting LPAR1, and the expression levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot. (E, F) Western blot analysis was performed to assess the expression levels of AKT and phosphorylated AKT (p-AKT). (G, H) DU145 cells were treated with 2 μM LY294002 (AKT pathway inhibitor), and the protein levels of AKT, phosphorylated AKT (p-AKT), N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. Band intensities were quantified using ImageJ software and normalized to actin. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Journal: Frontiers in Immunology

    Article Title: Identify GDPD3 as a key regulator of epithelial–mesenchymal transition and prostate adenocarcinoma progression via the LPA/LPAR1/AKT axis: transcriptomic and experimental study

    doi: 10.3389/fimmu.2025.1637325

    Figure Lengend Snippet: LPAR1 knockdown and AKT inhibition attenuate LPA-induced EMT. (A, B) LPAR1 was knocked down, and knockdown efficiency was subsequently validated. (C, D) DU145 cells were transfected with siRNA targeting LPAR1, and the expression levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot. (E, F) Western blot analysis was performed to assess the expression levels of AKT and phosphorylated AKT (p-AKT). (G, H) DU145 cells were treated with 2 μM LY294002 (AKT pathway inhibitor), and the protein levels of AKT, phosphorylated AKT (p-AKT), N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. Band intensities were quantified using ImageJ software and normalized to actin. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: The DU145 human prostate cancer cell line was obtained from the American Type Culture Collection (ATCC) in February 2025.

    Techniques: Knockdown, Inhibition, Transfection, Expressing, Western Blot, Software