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prostate epithelial cell line  (ATCC)


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    ATCC prostate epithelial cell line
    Prostate Epithelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 658 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/prostate epithelial cell line/product/ATCC
    Average 99 stars, based on 658 article reviews
    prostate epithelial cell line - by Bioz Stars, 2026-06
    99/100 stars

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    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).
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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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    Procell Inc human prostate epithelial cell line rwpe 1
    Epithelial ROS-ZNF24 axis drives MIF transcription and promotes CD74-dependent M1 macrophage polarization. (A–E) CD74 knockdown attenuates MIF-induced M1 macrophage polarization, as assessed by CD86 and iNOS expression (A–B), proinflammatory cytokine secretion (C), and flow cytometry analysis of F4/80 + CD86 + macrophages (D–E). (F–H) LPS stimulation induces MIF mRNA expression (F), protein expression (G), and secretion (H) <t>in</t> <t>RWPE-1</t> prostate epithelial cells. (I–K) Transwell co-culture system showing that LPS-stimulated prostate epithelial cells promote M1 polarization and cytokine secretion in iBMDMs, which is suppressed by the MIF inhibitor ISO-1. (L–M) Increased epithelial oxidative stress in EAP mice and LPS-stimulated RWPE-1 cells, indicated by 8-OHdG staining (L) and intracellular ROS levels (M), respectively; NAC effectively reduces ROS accumulation. (N–O) ROS scavenging with NAC suppresses epithelial MIF expression and attenuates M1 marker expression in co-cultured macrophages. (P–T) ZNF24 is induced by epithelial ROS and directly regulates MIF transcription, as shown by ZNF24 expression (P), ZNF24 knockdown (Q), predicted ZNF24 binding motifs in the MIF promoter (R), and ChIP assays demonstrating enhanced ZNF24 binding upon LPS stimulation (S–T). Data are presented as mean ± SD. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001. Abbreviations: iBMDMs, immortalized bone marrow-derived macrophages; RWPE-1, human prostate epithelial cell line; siCD74, small interfering RNA targeting CD74; LPS, lipopolysaccharide; NAC, N-acetylcysteine; ROS, reactive oxygen species.
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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

    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

    Epithelial ROS-ZNF24 axis drives MIF transcription and promotes CD74-dependent M1 macrophage polarization. (A–E) CD74 knockdown attenuates MIF-induced M1 macrophage polarization, as assessed by CD86 and iNOS expression (A–B), proinflammatory cytokine secretion (C), and flow cytometry analysis of F4/80 + CD86 + macrophages (D–E). (F–H) LPS stimulation induces MIF mRNA expression (F), protein expression (G), and secretion (H) in RWPE-1 prostate epithelial cells. (I–K) Transwell co-culture system showing that LPS-stimulated prostate epithelial cells promote M1 polarization and cytokine secretion in iBMDMs, which is suppressed by the MIF inhibitor ISO-1. (L–M) Increased epithelial oxidative stress in EAP mice and LPS-stimulated RWPE-1 cells, indicated by 8-OHdG staining (L) and intracellular ROS levels (M), respectively; NAC effectively reduces ROS accumulation. (N–O) ROS scavenging with NAC suppresses epithelial MIF expression and attenuates M1 marker expression in co-cultured macrophages. (P–T) ZNF24 is induced by epithelial ROS and directly regulates MIF transcription, as shown by ZNF24 expression (P), ZNF24 knockdown (Q), predicted ZNF24 binding motifs in the MIF promoter (R), and ChIP assays demonstrating enhanced ZNF24 binding upon LPS stimulation (S–T). Data are presented as mean ± SD. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001. Abbreviations: iBMDMs, immortalized bone marrow-derived macrophages; RWPE-1, human prostate epithelial cell line; siCD74, small interfering RNA targeting CD74; LPS, lipopolysaccharide; NAC, N-acetylcysteine; ROS, reactive oxygen species.

    Journal: Redox Biology

    Article Title: Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF–NF–κB pathway in chronic nonbacterial prostatitis

    doi: 10.1016/j.redox.2026.104042

    Figure Lengend Snippet: Epithelial ROS-ZNF24 axis drives MIF transcription and promotes CD74-dependent M1 macrophage polarization. (A–E) CD74 knockdown attenuates MIF-induced M1 macrophage polarization, as assessed by CD86 and iNOS expression (A–B), proinflammatory cytokine secretion (C), and flow cytometry analysis of F4/80 + CD86 + macrophages (D–E). (F–H) LPS stimulation induces MIF mRNA expression (F), protein expression (G), and secretion (H) in RWPE-1 prostate epithelial cells. (I–K) Transwell co-culture system showing that LPS-stimulated prostate epithelial cells promote M1 polarization and cytokine secretion in iBMDMs, which is suppressed by the MIF inhibitor ISO-1. (L–M) Increased epithelial oxidative stress in EAP mice and LPS-stimulated RWPE-1 cells, indicated by 8-OHdG staining (L) and intracellular ROS levels (M), respectively; NAC effectively reduces ROS accumulation. (N–O) ROS scavenging with NAC suppresses epithelial MIF expression and attenuates M1 marker expression in co-cultured macrophages. (P–T) ZNF24 is induced by epithelial ROS and directly regulates MIF transcription, as shown by ZNF24 expression (P), ZNF24 knockdown (Q), predicted ZNF24 binding motifs in the MIF promoter (R), and ChIP assays demonstrating enhanced ZNF24 binding upon LPS stimulation (S–T). Data are presented as mean ± SD. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001. Abbreviations: iBMDMs, immortalized bone marrow-derived macrophages; RWPE-1, human prostate epithelial cell line; siCD74, small interfering RNA targeting CD74; LPS, lipopolysaccharide; NAC, N-acetylcysteine; ROS, reactive oxygen species.

    Article Snippet: The iBMDM cell line (a murine immortalized macrophage line) was kindly provided by academician Feng Shao, and the human prostate epithelial cell line RWPE-1 (Cat. No. CL-0200, Procell) was obtained from Procell. iBMDM cells were cultured in high-glucose DMEM containing 10 % FBS and 1 % penicillin-streptomycin and passaged as needed.

    Techniques: Knockdown, Expressing, Flow Cytometry, Co-Culture Assay, Staining, Marker, Cell Culture, Binding Assay, Derivative Assay, Small Interfering RNA