作者: Hubert Pakula , Dongxi Xiang , Zhe Li
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摘要: Prostate cancer (PCa) is one of the most common cancers and among leading causes deaths for men in industrialized countries. It has long been recognized that prostate an androgen-dependent organ PCa disease. Androgen action mediated by androgen receptor (AR). deprivation therapy (ADT) standard treatment metastatic PCa. However, almost all advanced cases progress to castration-resistant (CRPC) after a period ADT. A variety mechanisms progression from CRPC under ADT have postulated, but it remains largely unclear as when how castration resistance arises within tumors. In addition, AR signaling may be modulated extracellular factors which are cysteine-rich glycoproteins WNTs. The WNTs capable through several pathways, best-characterized being canonical WNT/β-catenin/TCF-mediated pathway. Recent studies sequencing genomes revealed cells frequently harbor mutations major components WNT/β-catenin Moreover, finding interaction between β-catenin suggests possible mechanism cross talk WNT androgen/AR pathways. this review, we discuss current knowledge both pathways development tumorigenesis, their during CRPC. We also review therapeutic application drugs target Finally, extend our mammary gland system breast cancer. highlight role its with these two hormone-related types highly context-dependent.