miR-30 functions as an oncomiR in gastric cancer cells through regulation of P53-mediated mitochondrial apoptotic pathway

The present study was designed to investigate the role of miR-30 in the development of Gastric cancer (GC). miR-30 expression was increased in GC tissues and cell lines. Downregulation of miR-30 inhibited cell proliferation and promoted apoptosis in HGC-27 cells. Upregulation of miR-30 enhanced the proliferation and inhibited apoptosis. P53 expression was decreased in GC tissues. P53 expression was correlated with miR-30 expression. Downregulation of miR-30 increased P53 expression. Knockdown of P53 inhibited miR-30-inhibitor-induced suppression of cell proliferation and increase of apoptosis. Downregulation of miR-30 increased ROS generation which was inhibited by shP53. miR-30 inhibitors induced a decrease in mitochondrial oxygen consumption, cytoplasmic release of cytochrome c, and activation of Caspase 3 and 9, activating mitochondrial apoptotic pathway. Downregulation of P53 and N-acetyl-cysteine suppressed miR-30 inhibitors-activated mitochondrial dysfunction and apoptotic events. In conclusion, we identified that miR-30 functioned as a potential oncomiR through P53/ROS-mediated regulation of mitochondrial apoptotic pathway.

miR-30 functions as a potential oncomiR in GC through P53/ROS-mediated regulation of mitochondrial apoptotic pathway.