MicroRNA-320a suppresses tumor cell growth and invasion of human breast cancer by targeting insulin-like growth factor 1 receptor

摘要

The present study was performed to investigate the biological functions of microRNA-320a in human breast cancer and the underlying mechanisms. MicroRNA-320a expression was downregulated in human breast cancer, compared with the normal control. Overexpression of microRNA-320a induced apoptosis, and inhibited cell viability and invasion in MDA-MB-231cells while downregulation of microRNA-320a reduced apoptosis, and increased cell viability and invasion in MDA-MB-231 cells. Then, overexpression of microRNA-320a suppressed insulin-like growth factor 1 receptor (IGF-1R), p-AKt and cyclin D1 protein expression in MDA-MB-231cells. In addition, the downregulation of microRNA-320a induced IGF-1R, p-Akt and cyclin D1 protein expression in MDA-MB-231cells. Furthermore, the IGF-1R inhibitor increased the effects of microRNA-320a on the apoptosis of MDA-MB-231 cells. The p-Akt inhibitor (MK 2206 dihydrochloride, 2.5 nM) increased the effects of microRNA-320a on the apoptosis of MDA-MB-231 cells. These results revealed that microRNA-320a suppresses tumor cell growth and invasion of human breast cancer by targeting IGF-1R.