Matches in SemOpenAlex for { <https://semopenalex.org/work/W132230351> ?p ?o ?g. }
- W132230351 endingPage "246" @default.
- W132230351 startingPage "229" @default.
- W132230351 abstract "Androgen ablation therapy remains a highly effective modality for controlling early-stage prostate cancer. However, prostate cancers ultimately fail such therapy as the tumor epithelium progresses to a state of androgen independence, despite retaining high levels of the androgen receptor (AR). Substantial research effort is currently focused on exploring the molecular basis for escape from androgen dependence. Recent evidence overwhelmingly support that AR becomes constitutively activated in prostate carcinomas, at least partly through enhanced activity of kinases or AR-binding partners. Similarly, the activity of TGF-β which in prostate epithelium is believed to function as, a potent tumor suppressor has recently been shown to be modulated by AR, certain AR-binding partners, and the PI3K/Akt/mTOR pathway. We propose that TGF-β signaling through Smad3 is an important negative downstream effector of androgenic responses. In our model, activation of AR and PI3K/Akt/mTOR occurring in prostate cancer may promote disease progression through blocking the tumor suppressor activity of TGF-β/Smad3. This review thus provides new insight into the interactions among Smad3, AR, and Akt signaling pathways in controlling the progression of prostate cancer." @default.
- W132230351 created "2016-06-24" @default.
- W132230351 creator A5058446859 @default.
- W132230351 creator A5082651492 @default.
- W132230351 date "2008-01-01" @default.
- W132230351 modified "2023-09-26" @default.
- W132230351 title "Key Roles of TGF-β and Smad3 in Prostate Cancer" @default.
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