Knockdown of NCOA5 suppresses viability, migration and epithelial-mesenchymal transition, and induces adhesion of breast cancer cells.

Nuclear receptor coactivator 5 (NCOA5) has been reported to be involved in the regulation of several malignancies; however, to the best of our knowledge, its role in breast cancer is still unknown. The present study aimed to reveal the biological function of NCOA5 in breast cancer cells. NCOA5 expression in breast cancer tissues and cell lines was examined using reverse transcription-quantitative PCR and western blotting. Small interfering RNA (siRNA) against NCOA5 (siNCOA5) was transfected into MDA-MB-453 and MCF-7 cells to knock down NCOA5. MTT, transwell migration and cell adhesion assays were performed to determine cell viability, migration and adhesion abilities of breast cancer cells, respectively. In addition, the expression levels of N-cadherin, Vimentin and E-cadherin were examined by western blotting. It was revealed that NCOA5 expression was significantly increased in breast cancer tissues and cell lines. Knockdown of NCOA5 suppressed breast cancer cell viability and migration, and induced cell adhesion. Compared with those in cells transfected with non-targeting negative control siRNA, the protein expression levels of N-cadherin and Vimentin were significantly decreased, whereas the protein expression levels of E-cadherin were significantly increased in cells transfected with siNCOA5. The present study demonstrated that knockdown of NCOA5 suppressed cell viability and migration, induced cell adhesion, and inhibited epithelial-mesenchymal transition of breast cancer cells, indicating that NCOA5 may serve a tumor-promoting role in breast cancer.

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