Abstract
The current study aimed to evaluate the expression and role of miR-323a in the progression of bladder cancer (BC), thereby providing a theoretical basis and potential therapy methods for BC patients. Our data showed that miR-323a levels were significantly reduced in BC tissues compared with those of non-cancerous tissues. Meanwhile, miR-323a was significantly decreased in human BC cell lines (T24, J82, TCCSUP, RT-112) than that in human normal bladder epithelial cell line SV-HUC-1. Furthermore, inhibition of miR-323a markedly enhanced the migration and invasive capacity of T24 and TCCSUP cells. Moreover, overexpression of miR-323a significantly prompted the apoptosis of BC cells. Dual luciferase reporter assay and western blot analysis confirmed that c-Met was a target gene of miR-323a. More importantly, upregulation of c-Met significantly prompted BC cell proliferation mainly as a result of the enhanced level of phosphorylation of AKT. This effect could be abolished when c-Met was silenced in BC cells. In summary, reduced miR-323a expression in BC contributed to enhanced BC cell proliferation and migration mainly by targeting c-Met.