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- W2017223556 abstract "Abstract BACKGROUND Lethal prostate cancers often become androgen‐independent due to androgen receptor (AR) overexpression. The role of cadmium in prostate tumor progression was determined. METHODS Control and cadmium‐transformed prostate epithelial cells (CTPE) were compared for steroid‐induced proliferation, steroid receptor expression, and androgen metabolism. RESULTS CTPE cells showed rapid proliferation in complete medium and sustained proliferation in steroid‐reduced medium. Androgens stimulated significantly less cell proliferation and AR‐related genes expression in CTPE cells. 5α‐Dihydrotestosterone increased PSA expression more effectively in control cells. Flutamide reduced 5α‐dihydrotestosterone‐stimulated growth less effectively in CTPE cells compared to control. CTPE cells showed decreased p27 expression. Estrogen receptors were overexpressed and estradiol markedly stimulated proliferation in CTPE cells. In CTPE cells 5α‐aromatase was markedly increased, while 5α‐reductase was decreased. CONCLUSIONS Cadmium‐induced malignant transformation stimulates androgen independence, unrelated to AR expression or activity. Increased estrogen receptor and 5α‐aromatase expression suggest estrogen signaling may be critical to this process. Prostate © 2006 Wiley‐Liss, Inc." @default.
- W2017223556 created "2016-06-24" @default.
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- W2017223556 date "2006-10-30" @default.
- W2017223556 modified "2023-10-15" @default.
- W2017223556 title "Estrogen signaling and disruption of androgen metabolism in acquired androgen-independence during cadmium carcinogenesis in human prostate epithelial cells" @default.
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- W2017223556 doi "https://doi.org/10.1002/pros.20479" @default.
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