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human non tumoral prostate epithelial cells  (ATCC)


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    ATCC human non tumoral prostate epithelial cells
    Human Non Tumoral Prostate Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 530 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 530 article reviews
    human non tumoral prostate epithelial cells - by Bioz Stars, 2026-05
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    ATCC human prostate epithelial cancer cell line
    ( a ) A schematic workflow illustrating the preclinical therapeutic procedure. Two weeks after subcutaneous inoculation and in vivo uptake of PC3/PSC27 recombinants, severe combined immunodeficient (M-NSG) mice were subject to either single agent or combinatorial treatment in a metronomic schedule of several cycles. The illustration was created in BioRender. ( b ) Comparative statistics of tumor end volumes. PC3 cancer cells were inoculated either alone or combined with PSC27 stromal cells before being implanted subcutaneously to the hind flank of M-NSG animals, which were administered with MIT and SAA, either alone or in combination. ( c ) Representative images of in vivo senescence in tumor foci by SA-β-gal staining. Scale bar, 50 μm. ( d ) Comparative statistics of tumor senescence as described in ( c ). ( e ) Transcriptional analysis of a subset of SASP factors expressed in <t>epithelial</t> vs. stromal cells acquired from tumor foci after laser capture microdissection (LCM) to isolate stromal and cancer cells, respectively. Signals were normalized to that of the sample with lowest value in the placebo group. ( f ) Transcriptional analysis of SASP factors and two canonical senescence biomarkers p16 INK4a and p21 CIP1 . ( g ) Statistical assessment of DDR and cellular apoptosis in tumors. Values are shown as the percentage of cells positively stained by IF or IHC specific to γH2AX or cleaved caspase 3 (CCL3), respectively. ( h ) Representative images of IHC staining for CCL3 at the completion of treatment regimens. Scale bar, 50 μm. ( i ) Comparative survival of animals sacrificed upon development of advanced bulky disease. Survival duration was calculated from tissue recombinant injection until death. P values were calculated by a two-sided log-rank (Mantel-Cox) test. DDR, DNA damage response. IF, immunofluorescence. IHC, immunohistochemistry. Data in b , d , e , f and g are shown as mean ± SD and representative of 3 independent biological replicates, with P values calculated by Student’s t -tests. ^, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
    Human Prostate Epithelial Cancer Cell Line, 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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    ( a ) A schematic workflow illustrating the preclinical therapeutic procedure. Two weeks after subcutaneous inoculation and in vivo uptake of PC3/PSC27 recombinants, severe combined immunodeficient (M-NSG) mice were subject to either single agent or combinatorial treatment in a metronomic schedule of several cycles. The illustration was created in BioRender. ( b ) Comparative statistics of tumor end volumes. PC3 cancer cells were inoculated either alone or combined with PSC27 stromal cells before being implanted subcutaneously to the hind flank of M-NSG animals, which were administered with MIT and SAA, either alone or in combination. ( c ) Representative images of in vivo senescence in tumor foci by SA-β-gal staining. Scale bar, 50 μm. ( d ) Comparative statistics of tumor senescence as described in ( c ). ( e ) Transcriptional analysis of a subset of SASP factors expressed in <t>epithelial</t> vs. stromal cells acquired from tumor foci after laser capture microdissection (LCM) to isolate stromal and cancer cells, respectively. Signals were normalized to that of the sample with lowest value in the placebo group. ( f ) Transcriptional analysis of SASP factors and two canonical senescence biomarkers p16 INK4a and p21 CIP1 . ( g ) Statistical assessment of DDR and cellular apoptosis in tumors. Values are shown as the percentage of cells positively stained by IF or IHC specific to γH2AX or cleaved caspase 3 (CCL3), respectively. ( h ) Representative images of IHC staining for CCL3 at the completion of treatment regimens. Scale bar, 50 μm. ( i ) Comparative survival of animals sacrificed upon development of advanced bulky disease. Survival duration was calculated from tissue recombinant injection until death. P values were calculated by a two-sided log-rank (Mantel-Cox) test. DDR, DNA damage response. IF, immunofluorescence. IHC, immunohistochemistry. Data in b , d , e , f and g are shown as mean ± SD and representative of 3 independent biological replicates, with P values calculated by Student’s t -tests. ^, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    Procell Inc human normal prostate epithelial cells rwpe 1
    Integrin-β1 served as a key mechanoreceptor mediating the anti-ferroptotic action of Li-ESWT. (A–E) Western blot analysis of Integrin-β1, NRF2, and the ferroptosis-related proteins xCT and GPX4 <t>in</t> <t>RWPE-1</t> cells was performed to evaluate the effect of Li-ESWT-mediated Integrin-β1 activation on NRF2-xCT/GPX4 axis. (F–I) Lipid peroxidation and intracellular iron levels were assessed by flow cytometry using the C11 BODIPY and RhoNOX-6 probes, respectively, to evaluate the occurrence of ferroptosis following Li-ESWT, Integrin-β1 knockdown, or ferroptosis inhibitor Fer-1 treatment. Data were presented as mean±standard deviation. Li-ESWT: low-intensity extracorporeal shock wave therapy, Fer-1: Ferrostatin-1, LPS: lipopolysaccharide. * p<0.05, ** p<0.01, *** p<0.001.
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    Integrin-β1 served as a key mechanoreceptor mediating the anti-ferroptotic action of Li-ESWT. (A–E) Western blot analysis of Integrin-β1, NRF2, and the ferroptosis-related proteins xCT and GPX4 <t>in</t> <t>RWPE-1</t> cells was performed to evaluate the effect of Li-ESWT-mediated Integrin-β1 activation on NRF2-xCT/GPX4 axis. (F–I) Lipid peroxidation and intracellular iron levels were assessed by flow cytometry using the C11 BODIPY and RhoNOX-6 probes, respectively, to evaluate the occurrence of ferroptosis following Li-ESWT, Integrin-β1 knockdown, or ferroptosis inhibitor Fer-1 treatment. Data were presented as mean±standard deviation. Li-ESWT: low-intensity extracorporeal shock wave therapy, Fer-1: Ferrostatin-1, LPS: lipopolysaccharide. * p<0.05, ** p<0.01, *** p<0.001.
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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.
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    ATCC prostate epithelial cell line
    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.
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    ( a ) A schematic workflow illustrating the preclinical therapeutic procedure. Two weeks after subcutaneous inoculation and in vivo uptake of PC3/PSC27 recombinants, severe combined immunodeficient (M-NSG) mice were subject to either single agent or combinatorial treatment in a metronomic schedule of several cycles. The illustration was created in BioRender. ( b ) Comparative statistics of tumor end volumes. PC3 cancer cells were inoculated either alone or combined with PSC27 stromal cells before being implanted subcutaneously to the hind flank of M-NSG animals, which were administered with MIT and SAA, either alone or in combination. ( c ) Representative images of in vivo senescence in tumor foci by SA-β-gal staining. Scale bar, 50 μm. ( d ) Comparative statistics of tumor senescence as described in ( c ). ( e ) Transcriptional analysis of a subset of SASP factors expressed in epithelial vs. stromal cells acquired from tumor foci after laser capture microdissection (LCM) to isolate stromal and cancer cells, respectively. Signals were normalized to that of the sample with lowest value in the placebo group. ( f ) Transcriptional analysis of SASP factors and two canonical senescence biomarkers p16 INK4a and p21 CIP1 . ( g ) Statistical assessment of DDR and cellular apoptosis in tumors. Values are shown as the percentage of cells positively stained by IF or IHC specific to γH2AX or cleaved caspase 3 (CCL3), respectively. ( h ) Representative images of IHC staining for CCL3 at the completion of treatment regimens. Scale bar, 50 μm. ( i ) Comparative survival of animals sacrificed upon development of advanced bulky disease. Survival duration was calculated from tissue recombinant injection until death. P values were calculated by a two-sided log-rank (Mantel-Cox) test. DDR, DNA damage response. IF, immunofluorescence. IHC, immunohistochemistry. Data in b , d , e , f and g are shown as mean ± SD and representative of 3 independent biological replicates, with P values calculated by Student’s t -tests. ^, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: bioRxiv

    Article Title: Salvianolic acids are natural senolytics and increase lifespan in old age

    doi: 10.64898/2026.04.29.721790

    Figure Lengend Snippet: ( a ) A schematic workflow illustrating the preclinical therapeutic procedure. Two weeks after subcutaneous inoculation and in vivo uptake of PC3/PSC27 recombinants, severe combined immunodeficient (M-NSG) mice were subject to either single agent or combinatorial treatment in a metronomic schedule of several cycles. The illustration was created in BioRender. ( b ) Comparative statistics of tumor end volumes. PC3 cancer cells were inoculated either alone or combined with PSC27 stromal cells before being implanted subcutaneously to the hind flank of M-NSG animals, which were administered with MIT and SAA, either alone or in combination. ( c ) Representative images of in vivo senescence in tumor foci by SA-β-gal staining. Scale bar, 50 μm. ( d ) Comparative statistics of tumor senescence as described in ( c ). ( e ) Transcriptional analysis of a subset of SASP factors expressed in epithelial vs. stromal cells acquired from tumor foci after laser capture microdissection (LCM) to isolate stromal and cancer cells, respectively. Signals were normalized to that of the sample with lowest value in the placebo group. ( f ) Transcriptional analysis of SASP factors and two canonical senescence biomarkers p16 INK4a and p21 CIP1 . ( g ) Statistical assessment of DDR and cellular apoptosis in tumors. Values are shown as the percentage of cells positively stained by IF or IHC specific to γH2AX or cleaved caspase 3 (CCL3), respectively. ( h ) Representative images of IHC staining for CCL3 at the completion of treatment regimens. Scale bar, 50 μm. ( i ) Comparative survival of animals sacrificed upon development of advanced bulky disease. Survival duration was calculated from tissue recombinant injection until death. P values were calculated by a two-sided log-rank (Mantel-Cox) test. DDR, DNA damage response. IF, immunofluorescence. IHC, immunohistochemistry. Data in b , d , e , f and g are shown as mean ± SD and representative of 3 independent biological replicates, with P values calculated by Student’s t -tests. ^, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: The human prostate epithelial cancer cell line, PC3, was from ATCC and cultured with F-12K media (10% FBS).

    Techniques: In Vivo, Staining, Laser Capture Microdissection, Immunohistochemistry, Recombinant, Injection, Immunofluorescence

    Integrin-β1 served as a key mechanoreceptor mediating the anti-ferroptotic action of Li-ESWT. (A–E) Western blot analysis of Integrin-β1, NRF2, and the ferroptosis-related proteins xCT and GPX4 in RWPE-1 cells was performed to evaluate the effect of Li-ESWT-mediated Integrin-β1 activation on NRF2-xCT/GPX4 axis. (F–I) Lipid peroxidation and intracellular iron levels were assessed by flow cytometry using the C11 BODIPY and RhoNOX-6 probes, respectively, to evaluate the occurrence of ferroptosis following Li-ESWT, Integrin-β1 knockdown, or ferroptosis inhibitor Fer-1 treatment. Data were presented as mean±standard deviation. Li-ESWT: low-intensity extracorporeal shock wave therapy, Fer-1: Ferrostatin-1, LPS: lipopolysaccharide. * p<0.05, ** p<0.01, *** p<0.001.

    Journal: The World Journal of Men's Health

    Article Title: Inhibition of Ferroptosis in Prostatitis Model by Low Intensity Extracorporeal Shock Wave Therapy through the Integrin-β1/NRF2 Axis

    doi: 10.5534/wjmh.250222

    Figure Lengend Snippet: Integrin-β1 served as a key mechanoreceptor mediating the anti-ferroptotic action of Li-ESWT. (A–E) Western blot analysis of Integrin-β1, NRF2, and the ferroptosis-related proteins xCT and GPX4 in RWPE-1 cells was performed to evaluate the effect of Li-ESWT-mediated Integrin-β1 activation on NRF2-xCT/GPX4 axis. (F–I) Lipid peroxidation and intracellular iron levels were assessed by flow cytometry using the C11 BODIPY and RhoNOX-6 probes, respectively, to evaluate the occurrence of ferroptosis following Li-ESWT, Integrin-β1 knockdown, or ferroptosis inhibitor Fer-1 treatment. Data were presented as mean±standard deviation. Li-ESWT: low-intensity extracorporeal shock wave therapy, Fer-1: Ferrostatin-1, LPS: lipopolysaccharide. * p<0.05, ** p<0.01, *** p<0.001.

    Article Snippet: Human normal prostate epithelial cells RWPE-1 (Procell) were cultured in Prostate Epithelial Cell Medium (ScienCell).

    Techniques: Western Blot, Activation Assay, Flow Cytometry, Knockdown, Standard Deviation

    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