Abstract
Abstract Estrogen-related receptors (ERRα,β,γ) which share significant homology with estrogen receptors, are orphan nuclear receptors and constitutively transactivated without estrogen-binding. Among the three subtypes, ERRα has been characterized to play a pivotal role in diverse aspects of energy homeostasis, including oxidative phosphorylation and mitochondrial biogenesis, via its transcriptional regulation of target genes. Expression studies in clinical tumor tissues show that ERRα expression is positively associated with a few hormone-dependent cancers, including breast, ovarian and endometrial cancers, and has been proposed to be useful as a prognostic marker for these cancers. We have previously reported that ERRα displays a ubiquitous expression pattern in various prostatic cell lines and an apparent elevated expression in high grade prostate cancer. However, its exact functional roles and prognostic value in prostate cancer still remains unclear. In this study, we analyzed the functional significance of ERRα in prostate cancer cell growth regulation by its stable expression in a hormone-sensitive prostate cancer cell line LNCaP. Our results showed that stable expression of ERRα in LNCaP cells could enhance their in vitro cell proliferation, adhesion to fibronectin, invasion and colony formation capacities of LNCaP cells under both normoxia and hypoxia condition (1% O2), while such in vitro growth phenotypes could be suppressed by an ERRα specific antagonist XCT790, suggesting that ERRα-induced growth phenotypes were ERRα specific. Moreover, under hypoxia condition, stable ERRα over-expression could stabilize HIF1α protein, up-regulate VEGF expression with an ERRα dose dependent pattern. Taken together, our results showed that ERRα over expression promotes hypoxic growth of prostate cancer cells. (This study is supported by a RGC General Research Fund CUHK461009) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4543. doi:10.1158/1538-7445.AM2011-4543
Sign-in/Register to access full text options 
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 callDisclaimer: 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.
