MicroRNA‑320a suppresses tumor cell growth and invasion of human breast cancer by targeting insulin‑like growth factor1 receptor.

Abstract

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 factor1 receptor (IGF‑1R), p‑AKt and cyclinD1 protein expression in MDA‑MB‑231cells. In addition, the downregulation of microRNA‑320a induced IGF‑1R, p‑Akt and cyclinD1 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.