Crosstalking between androgen and PI3K/AKT signaling pathways in prostate cancer cells.

摘要: Both androgen action and PI3K medicated signaling pathways have been implicated in prostate tumorigenesis. Our receptor (AR) conditional transgenic mice developed murine prostatic intraepithelial neoplasia (mPIN) adenocarcinoma lesions recapitulating human cancer development progression. Role of AR contributing to malignancy was demonstrated by high degree expression atypical tumor cells mPIN as well the mice, but not adjacent normal tissue. Interestingly, reduced PI3K/Akt activation also appeared these mouse cells, suggesting an interaction between PI3K/AKT pathways. In this study, we further investigated interaction. We showed that depletion or knockdown results elevated levels active phosphorylated AKT cells. Castration Pten knock-out increased Akt, pS6 prostate. Using a series newly generated Ar reporter compound loss directly represses endogenous epithelial Moreover, Ar-mediated transcription purified Pten-null This study provides novel evidence demonstrating interplay pathways, introduces unique relevant models for studies context