Abstract: Objective To investigate the effect of miR-106b on the radiosensitivity of hepatoma cells and its possible mechanism. Methods The expression of miR-106b in human hepatoma cell lines HepG2, SMMC-7721, SK-HEP-1, Huh7 and normal hepatocyte QSG7701 were detected by qRT-PCR. The HepG2 cells were transfected with miR-106b siRNA(miR-106b down-regulated group), and the blank control group and negative control group were set up. After irradiated by different doses(0 Gy, 2 Gy, 4 Gy, 6 Gy, 8 Gy), cell plating efficiency(PE) and cell survival fraction(SF) were determined by cell clone formation assay. After irradiated by 6 Gy, the proliferation and apoptosis of cells in each group were detected by CCK-8 method and flow cytometry; the protein expressions of p-PI3K/PI3K, p-AKT/AKT, PCNA and Bax were detected by Western blot. Results Compared with QSG7701 cells, the expression level of miR-106b in HepG2, SMMC-7721, SK-HEP-1, and Huh7 cells was increased(all P<0.05), and the expression level of miR-106b in HepG2 cells was the highest. The results of clone formation experiment showed that PE and SF levels in HepG2 cells were reduced with the increase of irradiation dose (all P<0.05) after irradiated by different doses(0 Gy, 2 Gy, 4 Gy, 6 Gy, 8 Gy), and there was no statistical significance in PE and SF levels between 6 Gy and 8 Gy irradiation (both P>0.05). After 6 Gy irradiation , compared with the blank control group and the negative control group, the proliferation ability of HepG2 cells and the protein expression levels of p-PI3K/PI3K, p-AKT/AKT and PCNA in miR-106b down-regulated group were decreased(all P<0.05), while the apoptosis rate and the protein expression level of Bax were increased(all P<0.05). Conclusion The down-regulation of the expression of miR-106b can inhibit the proliferation and induce the apoptosis of HepG2 cells, while enhance the radiosensitivity, and the underlying mechanism may be related to the blocking of PI3K/AKT pathway activation.

Key words: Hepatoma, miR-106b, Radiosensitivity, PI3K/AKT pathway