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non malignant prostatic epithelial cell line rwpe 1  (ATCC)


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    ATCC non malignant prostatic epithelial cell line rwpe 1
    Non Malignant Prostatic Epithelial Cell Line Rwpe 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1031 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 1031 article reviews
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    ATCC non malignant prostatic epithelial cell line rwpe 1
    Non Malignant Prostatic Epithelial Cell Line Rwpe 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC prostatic epithelial cell line rwpe 1
    PhIP exposure induces cytotoxicity <t>in</t> <t>RWPE-1</t> cells and downregulates SLC14A1 expression in PC-3 cells. (A) Immunohistochemical staining of SLC14A1 in prostate cancer tissues and normal prostate tissues based on data from the HPA database. (B) Cell viability of RWPE-1 cells after treatment with increasing concentrations of PhIP for 48 h, as determined by CCK-8 assay. (C) Protein expression levels of SLC14A1 in PC-3 cells following PhIP treatment, as assessed by Western blot. (D) Relative mRNA expression levels of SLC14A1 in PC-3 cells after PhIP treatment, as determined by qRT-PCR (**p < 0.01, ***p < 0.001).
    Prostatic Epithelial Cell Line Rwpe 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC cells cell primary prostate atcc pcs 440 010
    PhIP exposure induces cytotoxicity <t>in</t> <t>RWPE-1</t> cells and downregulates SLC14A1 expression in PC-3 cells. (A) Immunohistochemical staining of SLC14A1 in prostate cancer tissues and normal prostate tissues based on data from the HPA database. (B) Cell viability of RWPE-1 cells after treatment with increasing concentrations of PhIP for 48 h, as determined by CCK-8 assay. (C) Protein expression levels of SLC14A1 in PC-3 cells following PhIP treatment, as assessed by Western blot. (D) Relative mRNA expression levels of SLC14A1 in PC-3 cells after PhIP treatment, as determined by qRT-PCR (**p < 0.01, ***p < 0.001).
    Cells Cell Primary Prostate Atcc Pcs 440 010, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    ATCC rwpe 1 prostate epithelial cells
    PhIP exposure induces cytotoxicity <t>in</t> <t>RWPE-1</t> cells and downregulates SLC14A1 expression in PC-3 cells. (A) Immunohistochemical staining of SLC14A1 in prostate cancer tissues and normal prostate tissues based on data from the HPA database. (B) Cell viability of RWPE-1 cells after treatment with increasing concentrations of PhIP for 48 h, as determined by CCK-8 assay. (C) Protein expression levels of SLC14A1 in PC-3 cells following PhIP treatment, as assessed by Western blot. (D) Relative mRNA expression levels of SLC14A1 in PC-3 cells after PhIP treatment, as determined by qRT-PCR (**p < 0.01, ***p < 0.001).
    Rwpe 1 Prostate Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC prostate cancer epithelial cell lines pc3
    PhIP exposure induces cytotoxicity <t>in</t> <t>RWPE-1</t> cells and downregulates SLC14A1 expression in PC-3 cells. (A) Immunohistochemical staining of SLC14A1 in prostate cancer tissues and normal prostate tissues based on data from the HPA database. (B) Cell viability of RWPE-1 cells after treatment with increasing concentrations of PhIP for 48 h, as determined by CCK-8 assay. (C) Protein expression levels of SLC14A1 in PC-3 cells following PhIP treatment, as assessed by Western blot. (D) Relative mRNA expression levels of SLC14A1 in PC-3 cells after PhIP treatment, as determined by qRT-PCR (**p < 0.01, ***p < 0.001).
    Prostate Cancer Epithelial Cell Lines Pc3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC prostatic epithelial cells wpmy1
    a A qPCR was applied to detect circPHGDH expression in paired PCa and para-PCa tissues ( n = 51). b The circPHGDH expression was measured by qPCR in normal cells <t>(WPMY1)</t> and PCa cell lines (22Rv1, DU145, DuCaP, VCaP, LNCaP and C4-2). c The circPHGDH expression detected by qPCR to confirm successful transfection. d – i After circPHGDH was knocked down or overexpressed, cell proliferation ( d ) was analyzed by colony formation analysis; migration ( e ) and invasion ( f ) were estimated by Transwell assay; E-cadherin and N-cadherin protein levels ( g ) were examined using western blotting; and ECAR ( h ) and OCR ( i ) were measured using Seahorse assay to reflect glycolytic fluxes. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the oe-nc group.
    Prostatic Epithelial Cells Wpmy1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC normal human prostate epithelial cells hprec
    Genistein and butein reduce cell viability in prostate cancer cells. ( A ) Chemical structures of GEN and BTN. ( B ) Viability of PC-3 prostate cancer cells and <t>HPrEC</t> following exposure to increasing concentrations of GEN or BTN for 24 or 48 h, evaluated using the MTT assay. ( C ) Cell viability measured by means of trypan blue exclusion under identical treatment conditions. Results are normalized to untreated controls, and IC 50 values were calculated from 48 h treatment data where indicated. Values represent the mean ± SD of at least three independent experiments; * p < 0.05 versus control. HPrEC: normal human prostate <t>epithelial</t> cells; GEN: genistein; BTN: butein; Conc.: concentration.
    Normal Human Prostate Epithelial Cells Hprec, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    PhIP exposure induces cytotoxicity in RWPE-1 cells and downregulates SLC14A1 expression in PC-3 cells. (A) Immunohistochemical staining of SLC14A1 in prostate cancer tissues and normal prostate tissues based on data from the HPA database. (B) Cell viability of RWPE-1 cells after treatment with increasing concentrations of PhIP for 48 h, as determined by CCK-8 assay. (C) Protein expression levels of SLC14A1 in PC-3 cells following PhIP treatment, as assessed by Western blot. (D) Relative mRNA expression levels of SLC14A1 in PC-3 cells after PhIP treatment, as determined by qRT-PCR (**p < 0.01, ***p < 0.001).

    Journal: Frontiers in Immunology

    Article Title: PhIP-driven prostate cancer involves key molecular regulators and immune microenvironment modulation

    doi: 10.3389/fimmu.2026.1782240

    Figure Lengend Snippet: PhIP exposure induces cytotoxicity in RWPE-1 cells and downregulates SLC14A1 expression in PC-3 cells. (A) Immunohistochemical staining of SLC14A1 in prostate cancer tissues and normal prostate tissues based on data from the HPA database. (B) Cell viability of RWPE-1 cells after treatment with increasing concentrations of PhIP for 48 h, as determined by CCK-8 assay. (C) Protein expression levels of SLC14A1 in PC-3 cells following PhIP treatment, as assessed by Western blot. (D) Relative mRNA expression levels of SLC14A1 in PC-3 cells after PhIP treatment, as determined by qRT-PCR (**p < 0.01, ***p < 0.001).

    Article Snippet: The human prostatic epithelial cell line RWPE-1 and the human prostate cancer cell line PC-3 were obtained from the American Type Culture Collection (ATCC).

    Techniques: Expressing, Immunohistochemical staining, Staining, CCK-8 Assay, Western Blot, Quantitative RT-PCR

    a A qPCR was applied to detect circPHGDH expression in paired PCa and para-PCa tissues ( n = 51). b The circPHGDH expression was measured by qPCR in normal cells (WPMY1) and PCa cell lines (22Rv1, DU145, DuCaP, VCaP, LNCaP and C4-2). c The circPHGDH expression detected by qPCR to confirm successful transfection. d – i After circPHGDH was knocked down or overexpressed, cell proliferation ( d ) was analyzed by colony formation analysis; migration ( e ) and invasion ( f ) were estimated by Transwell assay; E-cadherin and N-cadherin protein levels ( g ) were examined using western blotting; and ECAR ( h ) and OCR ( i ) were measured using Seahorse assay to reflect glycolytic fluxes. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the oe-nc group.

    Journal: Experimental & Molecular Medicine

    Article Title: A ESRP1/circPHGDH/miR-149/RAP1B positive feedback loop promotes the malignant behaviors and glycolysis of prostate cancer cell

    doi: 10.1038/s12276-026-01646-x

    Figure Lengend Snippet: a A qPCR was applied to detect circPHGDH expression in paired PCa and para-PCa tissues ( n = 51). b The circPHGDH expression was measured by qPCR in normal cells (WPMY1) and PCa cell lines (22Rv1, DU145, DuCaP, VCaP, LNCaP and C4-2). c The circPHGDH expression detected by qPCR to confirm successful transfection. d – i After circPHGDH was knocked down or overexpressed, cell proliferation ( d ) was analyzed by colony formation analysis; migration ( e ) and invasion ( f ) were estimated by Transwell assay; E-cadherin and N-cadherin protein levels ( g ) were examined using western blotting; and ECAR ( h ) and OCR ( i ) were measured using Seahorse assay to reflect glycolytic fluxes. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the oe-nc group.

    Article Snippet: Prostatic epithelial cells (WPMY1) and PCa cell lines (22Rv1, DU145, DuCaP, VCaP, LNCaP and C4-2), obtained from the American Type Culture Collection (ATCC), were cultured in Dulbecco’s modified Eagle medium (Thermo Fisher Scientific) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C in a 5% CO 2 .

    Techniques: Expressing, Transfection, Migration, Transwell Assay, Western Blot

    a Targeted miRNAs were chosen by a luciferase reporter analysis. b The predicted complementary sequences of circPHGDH and miR-149. c , d A dual-luciferase reporter assay ( c ) and RNA pull-down analysis ( d ) were determined for targeting relationship confirmation. e A qPCR was applied to test miR-149 expression in PCa cells after sh-circPHGDH or oe-circPHGDH transfection. f The MiR-149 expression in PCa tissues and para-PCa tissues was examined by qPCR ( n = 51). g The correlation of miR-149 and circPHGDH expression in PCa tissues was analyzed using Pearson correlation coefficient. h The MiR-149 expression in WPMY1 and PCa cell lines was tested by qPCR. i The location of circPHGDH and miR-149 in PCa cells was observed using FISH. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the oe-nc group.

    Journal: Experimental & Molecular Medicine

    Article Title: A ESRP1/circPHGDH/miR-149/RAP1B positive feedback loop promotes the malignant behaviors and glycolysis of prostate cancer cell

    doi: 10.1038/s12276-026-01646-x

    Figure Lengend Snippet: a Targeted miRNAs were chosen by a luciferase reporter analysis. b The predicted complementary sequences of circPHGDH and miR-149. c , d A dual-luciferase reporter assay ( c ) and RNA pull-down analysis ( d ) were determined for targeting relationship confirmation. e A qPCR was applied to test miR-149 expression in PCa cells after sh-circPHGDH or oe-circPHGDH transfection. f The MiR-149 expression in PCa tissues and para-PCa tissues was examined by qPCR ( n = 51). g The correlation of miR-149 and circPHGDH expression in PCa tissues was analyzed using Pearson correlation coefficient. h The MiR-149 expression in WPMY1 and PCa cell lines was tested by qPCR. i The location of circPHGDH and miR-149 in PCa cells was observed using FISH. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the oe-nc group.

    Article Snippet: Prostatic epithelial cells (WPMY1) and PCa cell lines (22Rv1, DU145, DuCaP, VCaP, LNCaP and C4-2), obtained from the American Type Culture Collection (ATCC), were cultured in Dulbecco’s modified Eagle medium (Thermo Fisher Scientific) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C in a 5% CO 2 .

    Techniques: Luciferase, Reporter Assay, Expressing, Transfection

    a The targets of miR-149 predicted using the miRDB, starbase and TargetScan databases are shown using Venn diagram. b The KEGG enrichment analysis of these targeted genes. c The predicted complementary sequences of RAP1B and miR-149. d , e Luciferase reporter ( d ) and RNA pull-down assays ( e ) were used to determine the targeting relationship. f , g qPCR ( f ) and western blotting ( g ) were applied to detect RAP1B expression after circPHGDH and miR-149 knockdown. h The RAP1B levels in PCa tissues and para-PCa tissues were detected by qPCR ( n = 51). i The correlation of miR-149 and RAP1B expression in PCa tissues were analyzed using Pearson correlation coefficient. j , k The RAP1B levels in WPMY1 and PCa cell lines were tested by qPCR ( j ) and western blotting ( k ). l The RAP1B-correlated genes were predicted using the LinkedOmics database. m The KEGG enrichment analysis of all RAP1B-correlated genes. n The 22Rv1 and VCap cells were transfected RAP1B overexpression plasmids, the protein levels of RAP1B, phosphorylated (p)-PI3K, PI3K, p-AKT and AKT were detected using western blotting. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the sh-circPHGDH + nc inhibitor group.

    Journal: Experimental & Molecular Medicine

    Article Title: A ESRP1/circPHGDH/miR-149/RAP1B positive feedback loop promotes the malignant behaviors and glycolysis of prostate cancer cell

    doi: 10.1038/s12276-026-01646-x

    Figure Lengend Snippet: a The targets of miR-149 predicted using the miRDB, starbase and TargetScan databases are shown using Venn diagram. b The KEGG enrichment analysis of these targeted genes. c The predicted complementary sequences of RAP1B and miR-149. d , e Luciferase reporter ( d ) and RNA pull-down assays ( e ) were used to determine the targeting relationship. f , g qPCR ( f ) and western blotting ( g ) were applied to detect RAP1B expression after circPHGDH and miR-149 knockdown. h The RAP1B levels in PCa tissues and para-PCa tissues were detected by qPCR ( n = 51). i The correlation of miR-149 and RAP1B expression in PCa tissues were analyzed using Pearson correlation coefficient. j , k The RAP1B levels in WPMY1 and PCa cell lines were tested by qPCR ( j ) and western blotting ( k ). l The RAP1B-correlated genes were predicted using the LinkedOmics database. m The KEGG enrichment analysis of all RAP1B-correlated genes. n The 22Rv1 and VCap cells were transfected RAP1B overexpression plasmids, the protein levels of RAP1B, phosphorylated (p)-PI3K, PI3K, p-AKT and AKT were detected using western blotting. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ## P < 0.01 versus the sh-circPHGDH + nc inhibitor group.

    Article Snippet: Prostatic epithelial cells (WPMY1) and PCa cell lines (22Rv1, DU145, DuCaP, VCaP, LNCaP and C4-2), obtained from the American Type Culture Collection (ATCC), were cultured in Dulbecco’s modified Eagle medium (Thermo Fisher Scientific) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C in a 5% CO 2 .

    Techniques: Luciferase, Western Blot, Expressing, Knockdown, Transfection, Over Expression

    Genistein and butein reduce cell viability in prostate cancer cells. ( A ) Chemical structures of GEN and BTN. ( B ) Viability of PC-3 prostate cancer cells and HPrEC following exposure to increasing concentrations of GEN or BTN for 24 or 48 h, evaluated using the MTT assay. ( C ) Cell viability measured by means of trypan blue exclusion under identical treatment conditions. Results are normalized to untreated controls, and IC 50 values were calculated from 48 h treatment data where indicated. Values represent the mean ± SD of at least three independent experiments; * p < 0.05 versus control. HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein; Conc.: concentration.

    Journal: Current Issues in Molecular Biology

    Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

    doi: 10.3390/cimb48030258

    Figure Lengend Snippet: Genistein and butein reduce cell viability in prostate cancer cells. ( A ) Chemical structures of GEN and BTN. ( B ) Viability of PC-3 prostate cancer cells and HPrEC following exposure to increasing concentrations of GEN or BTN for 24 or 48 h, evaluated using the MTT assay. ( C ) Cell viability measured by means of trypan blue exclusion under identical treatment conditions. Results are normalized to untreated controls, and IC 50 values were calculated from 48 h treatment data where indicated. Values represent the mean ± SD of at least three independent experiments; * p < 0.05 versus control. HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein; Conc.: concentration.

    Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: MTT Assay, Control, Concentration Assay

    Combined genistein and butein treatment impairs glycolytic metabolism in PC-3 cells. HPrEC and PC-3 cells were treated with GEN, BTN, or GEN/BTN for 48 h. ( A , B ) Extracellular lactate production and glucose consumption were quantified and normalized to control levels. Enzymatic activities of hexokinase (HK) and pyruvate dehydrogenase (PDH) were assessed following treatment. GEN/BTN co-treatment produced a pronounced suppression of glycolytic activity in PC-3 cells, whereas metabolic parameters in HPrEC cells remained largely unchanged. Data are shown as the mean ± SD (n = 3). Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein.

    Journal: Current Issues in Molecular Biology

    Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

    doi: 10.3390/cimb48030258

    Figure Lengend Snippet: Combined genistein and butein treatment impairs glycolytic metabolism in PC-3 cells. HPrEC and PC-3 cells were treated with GEN, BTN, or GEN/BTN for 48 h. ( A , B ) Extracellular lactate production and glucose consumption were quantified and normalized to control levels. Enzymatic activities of hexokinase (HK) and pyruvate dehydrogenase (PDH) were assessed following treatment. GEN/BTN co-treatment produced a pronounced suppression of glycolytic activity in PC-3 cells, whereas metabolic parameters in HPrEC cells remained largely unchanged. Data are shown as the mean ± SD (n = 3). Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein.

    Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Control, Produced, Activity Assay

    Genistein–butein co-treatment decreases ATP levels and clonogenic survival in PC-3 cells. ( A ) Intracellular ATP content was determined after 48 h exposure to GEN, BTN, or GEN/BTN, and expressed relative to control cells (n = 3 independent experiments). ( B ) Crystal violet staining images illustrating treatment-dependent changes in cell survival. ( C ) Quantitative analysis of crystal violet staining measured at 590 nm. Each dot represents an individual replicate, and data are presented as mean ± SD (total n = 8 pooled from at least three independent experiments). Following GEN/BTN co-treatment in PC-3 cells, a significant reduction in ATP production and cell survival was observed, while normal HPrEC cells showed minimal changes. Results represent the mean ± SD from three independent experiments. Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein.

    Journal: Current Issues in Molecular Biology

    Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

    doi: 10.3390/cimb48030258

    Figure Lengend Snippet: Genistein–butein co-treatment decreases ATP levels and clonogenic survival in PC-3 cells. ( A ) Intracellular ATP content was determined after 48 h exposure to GEN, BTN, or GEN/BTN, and expressed relative to control cells (n = 3 independent experiments). ( B ) Crystal violet staining images illustrating treatment-dependent changes in cell survival. ( C ) Quantitative analysis of crystal violet staining measured at 590 nm. Each dot represents an individual replicate, and data are presented as mean ± SD (total n = 8 pooled from at least three independent experiments). Following GEN/BTN co-treatment in PC-3 cells, a significant reduction in ATP production and cell survival was observed, while normal HPrEC cells showed minimal changes. Results represent the mean ± SD from three independent experiments. Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein.

    Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Control, Staining

    Genistein–butein co-treatment promotes apoptosis and suppresses AKT/ERK signaling in PC-3 cells. ( A ) Apoptotic cell populations were evaluated using Annexin V and viability staining after 48 h treatment. Representative dot plots are shown for HPrEC and PC-3 cells. ( B ) Expression levels of hexokinase II and PDH were analyzed by means of Western blotting, with β-actin serving as a loading control. Corresponding densitometric analyses are presented. ( C ) Phosphorylation status of AKT and ERK, along with levels of cleaved caspase-3 and cleaved PARP, was examined by Western blot analysis. GEN/BTN co-treatment selectively inhibited survival signaling and enhanced apoptotic marker cleavage in PC-3 cells. Data are presented as the mean ± SD. Statistical significance is indicated. Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein; PDH: pyruvate dehydrogenase.

    Journal: Current Issues in Molecular Biology

    Article Title: Genistein–Butein Co-Treatment Suppresses Glycolytic Metabolism and Induces Apoptotic Signaling in PC-3 Prostate Cancer Cells

    doi: 10.3390/cimb48030258

    Figure Lengend Snippet: Genistein–butein co-treatment promotes apoptosis and suppresses AKT/ERK signaling in PC-3 cells. ( A ) Apoptotic cell populations were evaluated using Annexin V and viability staining after 48 h treatment. Representative dot plots are shown for HPrEC and PC-3 cells. ( B ) Expression levels of hexokinase II and PDH were analyzed by means of Western blotting, with β-actin serving as a loading control. Corresponding densitometric analyses are presented. ( C ) Phosphorylation status of AKT and ERK, along with levels of cleaved caspase-3 and cleaved PARP, was examined by Western blot analysis. GEN/BTN co-treatment selectively inhibited survival signaling and enhanced apoptotic marker cleavage in PC-3 cells. Data are presented as the mean ± SD. Statistical significance is indicated. Statistical significance is indicated by asterisks (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001). HPrEC: normal human prostate epithelial cells; GEN: genistein; BTN: butein; PDH: pyruvate dehydrogenase.

    Article Snippet: Human prostate cancer PC-3 cells and normal human prostate epithelial cells (HPrEC) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Staining, Expressing, Western Blot, Control, Phospho-proteomics, Marker