Effect of microRNA-27a-3p on proliferation, apoptosis and cell cycle of hepatoma cells

Abstract

Objective: To investigate the effect of miR-27a-3p on proliferation, apoptosis and cell cycle of hepatoma cells. Methods: A quantitative real-time polymerase chain reaction (qPCR) was used to detect differential expression of miR-27a-3p in normal hepatic epithelial cells (L02) and hepatoma cells (HepG2 and PLC). Cell experiment was divided into four groups: HepG2 overexpression cells, Mi-27a-3p overexpression group (Mi-27a) and negative control group (Mi-Con); PLC knockdown cells, Mi-27a-3p knockdown group (Mi-inhibitor-27a) and negative control group (Mi-inhibitor-Con). The expression of microRNA-27a-3p in each group after transfection was detected by qPCR analysis. MTT assay was used to detect the cell proliferation. Flow cytometry was used to detect the apoptosis and cell cycle. One-way ANOVA was used for multiple comparisons, and t-test was used to compare two groups. Results: qPCR results showed that the expression levels of miR-27a-3p in L02, HepG2 and PLC increased sequentially, and the relative expression levels were 1.07 ± 0.04, 4.81 ± 0.64 and 11.31 ± 0.92, respectively (P < 0.05). MTT assay showed that the cell viability of HepG2 cells transfected with miR-27a-3p overexpression plasmid was significantly decreased compared with the negative control group (P < 0.05). The apoptosis assay showed that the apoptosis rate of miR-27a-3p overexpression group was higher than the negative control group (P < 0.05). The cell cycle results showed that the proportion of S phase cells in the miR-27a-3p overexpression cell group was significantly lower than the negative control group (P < 0.05). Furthermore, microRNA-27a-3p knockdown validation in PLC cells showed that MTT, apoptosis and cell cycle tests results were opposite to the results of HepG2 overexpression cells, and the differences were statistically significant (P < 0.05). Conclusion: miR-27a-3p can significantly inhibit the proliferation of hepatoma cells, promote cell apoptosis, alter the cell cycle distribution, and may become a potential target in hepatocellular carcinoma therapy.