Abstract
Abstract Triple-negative breast cancer(TNBC)is a major world health problem, accounting for more than 15% of breast cancer new cases each year. The 5-year survival rate for TNBC is approximately 54.5% and death usually occurs as a result of local invasion and regional metastases. A complete understanding of the molecular mechanisms that control the aggressive behavior of triple-negative breast cancer cells is essential in order to develop targeted therapies to manage the disease. Recent evidence has suggested a role of Androgen receptor (AR)in cellular motility and invasion. In this present study we examined the role of AR on the migration and invasion of triple-negative breast cancer cells. Detect the AR levels in 7 cell line of breast cancer cells including MCF-7, MDA-MB-157, MDA-MB-231, MDA-MB-435, MDA-MB-468, MDA-MB-549, HS-578T by Q-PCR, we demonstrate that AR is highly express in triple-negative breast cancer cells; shRNAs specific to AR have been generated and delivered into human breast cancer cells by lentiviral vectors. We showed that the total levels of AR can be decreased by AR shRNA and inhibit MDA-MB-231 cellular motility and large focal adhesion (FA) formation, the cell migration was determined by time-lapse cell migration assays, depletion of endogenous AR significantly reduced the velocity and directionality of cell migration, and strongly inhibited the net distance of cell migration, indicating that AR modulates cell migration by controlling the velocity and directionality of migration. We also showed that AR activation and the migration and invasion of MDA-MB-231 , MDA-MB-435, MDA-MB-468 can be strongly inhibited with commercially available AR blocker Bicalutamide by cell migration and invasion assay. These results suggest that AR in breast cancer cells is required for cellular migration and invasion. Citation Format: Qiao-dan ZHENG, Wenyuan Wu, Cai Huang. Androgen receptor is involved in the migration and invasion of triple-negative breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4060. doi:10.1158/1538-7445.AM2014-4060
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