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ABSTRACT: Background
Androgen deprivation therapies for the hormone-dependent stages of prostate cancer have become so effective that new forms of chemoresistant tumors are emerging in clinical practice, and require new targeted therapies in the metastatic setting. Yet there are important gaps in our understanding of the relevant transcriptional networks driving this process. Progression from localized to metastatic castration resistant prostate cancer (mCRPC) occurs as a result of accumulated resistance mechanisms that develop upon sustained androgen receptor (AR) suppression. Critical to this progression is the plastic nature by which prostate tumor cells transition from epithelial to mesenchymal states (EMT).Methods
Here, using prostate cancer cell lines with different AR composit
SUBMITTER: Shafran JS
PROVIDER: S-EPMC7855805 | biostudies-literature | 2021 Mar
REPOSITORIES: biostudies-literature