Abstract

Abstract Prostate cancer (PCa) is the most common non-skin cancer and the 3rd leading cause of cancer-related death in American men. Androgen ablation therapy has been the gold standard for treating advanced stage PCa since the 1960s. Initially, the PCa patients respond to hormone ablation very positively. However, over time these tumors almost always become resistant to androgen ablation therapy, and tumors begin to grow again. Recent studies found after failure of the new drugs that block androgen action, PCa has increased neuroendocrine phenotype. Understanding the mechanisms through which PCa cells gain neuroendocrine phenotype is critical for the development of novel therapeutics. Polycomb repressive complex are involved in early embryo development and carcinogenesis in several types of cancer including PCa. In this study, we evaluated the involvement of Polycomb proteins in neuroendocrine PCa. Using immunohistochemistry staining, we examined the expression of Polycomb protein EZH2 in advanced stage PCa. We found that EZH2 is highly expressed in both human and mouse neuroendocrine PCa. Also, we found when PCa cells are induced to undergo neuroendocrine differentiation, multiple Polycomb genes are induced. These data suggest that Polycomb genes play a role in the development of neuroendocrine PCa. Citation Format: Zachary Connelly, Shu Yang, Anthony Blankenship, Xiuping Yu. Role of polycomb proteins in neuroendocrine prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1514.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.