Inhibition of the androgen receptor induces a novel tumor promoter, ZBTB46, for prostate cancer metastasis

W-Y Chen, Y-C Tsai, M K Siu, H-L Yeh, C-L Chen, J J Yin, J Huang, Y-N Liu

研究成果: 雜誌貢獻文章

11 引文 斯高帕斯(Scopus)

摘要

Current therapeutic regimens for prostate cancer focus on targeting androgen receptor (AR) signaling. However, the AR is a key factor in luminal epithelium differentiation and was shown to have a role as a tumor suppressor. Thus, its inhibition may activate oncogenic pathways that contribute to metastatic castration-resistant prostate cancer (CRPC). Herein, we report a novel tumor promoter, ZBTB46, which is negatively regulated by AR signaling via microRNA (miR)-1-mediated downregulation. ZBTB46 is associated with malignant prostate cancer and is essential for metastasis. Its overexpression can overcome the antitumor effects of miR-1 and promote androgen-independent proliferation. We demonstrated that ZBTB46 can transcriptionally regulate SNAI1, a key epithelial-to-mesenchymal transition (EMT) driver, which could contribute to induction of the EMT after androgen-deprivation therapy and metastasis. Our findings are supportive of the model that disruption of AR's function may predispose prostate cancer to progress to metastatic CRPC.Oncogene advance online publication, 10 July 2017; doi:10.1038/onc.2017.226.
原文英語
頁(從 - 到)6213-6224
期刊Oncogene
DOIs
出版狀態打印前電子出版 - 七月 10 2017

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