Effects of MicroRNA-132 transfection on the proliferation and apoptosis of human liver cancer cells in vitro and in vivo.

Abstract

To observe the biological role and underlying mechanism of microRNA-132 (miR-132) in liver cancer cell proliferation and apoptosis. The expressions of miR-132 in the cancer tissue and their adjacent tissues from 45 liver cancer patients were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The biological effects of miR-132 transfection on human liver cancer MHCC97H cells were assessed by CCK-8 assay, flow cytometry,in vivo experiment in nude mice, and TUNEL test. Western blotting was used to detect the expressions of p-AKT, Survivin, and Caspase 3 in liver cancer cells. Immunohistochemistry was used to detect the positive expressions of Ki-67,Survivin,and Caspase 3 in the xenograft tumors. The expression level of miR-132 was found to be down-regulated in liver cancer tissues compared with the matched adjacent tissues (P<0.05). After transfection,the expression of miR-132 was significantly higher than blank control group and negative control group (P<0.05). The proliferation of liver cancer cells was inhibited significantly by miR-132 transfection (P<0.05). Transfection of miR-132 arrested cells in the G0/G1 phase and triggered apoptosis of MHCC97H cells (P<0.05). After miR-132 transfection,the expression of Caspase 3 was up-regulated, whereas the expressions of p-AKT and Survivin were down-regulated (P<0.05). In addition,the tumor weight in miR-132 transfection group was significantly decreased in comparison with blank control group and negative control group (P<0.05). Apoptosis occurred more frequently in the miR-132 transfection group than in control groups (P<0.05). Compared with the blank control group and negative control group, the miR-132 transfection group had significantly decreased expression of Survivin but increased positive expression of Ki-67 and Caspase 3(P<0.05). miR-132 is down-regulated in human liver cancer tissues miR-132 transfection can effectively inhibit proliferation and promote apoptosis of MHCC97H cells in vitro and in vivo. Therefore, miR-132 may become a new target in liver cancer treatment.