Effect of microRNA-181 on proliferation and apoptosis of hepatocellular carcinoma cells via regulation of phosphatase and tensin ho-molog deleted from chromosome 10

Objective To explore effect of microRNA (miRNA, miR)-181b on proliferation and apoptosis of hepatocellular carcinoma cells via regulation of phosphatase and tensin ho-molog deleted from chromosome 10 (PTEN). Methods miR-181b inhibitor and miR-181b NC were transfected into HepG2 cell by liposome Lipofectamine™3000. The expression of miR-181b was detected by real-time quantitative polymerase chain reaction (Real-time PCR). Cell viability was measured by methyl thiazol tetrazolium (MTT) assay. Cell clone ability was detected by cell clone formation test. Cell apoptosis and cell cycle was detected by flow cytometry. The expression of PTEN protein and mRNA was measured by Western blotting and Real-time PCR. Luciferase reporter analysis was performed. Results The expression of miR-181b in miR-181b inhibitor group (0.23±0.02) was lower than that in miR-181b NC group (1.00±0.01, P<0.05). Cell viability in miR-181b inhibitor group (0.37±0.03) was lower than that in miR-181b NC group (0.59±0.06, P<0.05). Clone formation test showed cell clone number in miR-181b inhibitor group (37.64±3.70) was lower than that in miR-181b NC group (132.56±12.37, P<0.05). Cell early apoptotic rate and late apoptotic rate in miR-181b inhibitor group was higher than that in miR-181b NC group (P<0.05). At the same time, compared with miR-181b NC group, cell cycle was made arrested at G1 phase (P<0.05), the expression of PTEN protein and mRNA was up-regulated in miR-181b inhibitor group (P<0.05), miR-181b inhibitor targeted regulation the expression of PTEN. Conclusion miR-181b inhibitor could inhibit HepG2 cell proliferation and induce cell apoptosis by targeting up-regulation expression of PTEN. Key words: Hepatocellular carcinoma; MicroRNA-181b; Phosphatase and tensin ho-molog deleted from chromosome 10; Proliferation; Apoptosis