miR-106b对肝癌细胞放疗敏感性的影响及其作用机制

目的 探讨miR-106b对肝癌细胞放疗敏感性的影响及其可能的作用机制.方法 采用qRT-PCR检测人肝癌细胞株HepG2、SMMC-7721、SK-HEP-1、Huh7及正常肝细胞株QSG7701 中miR-106b mRNA 的表达.用miR-106b siRNA转染HepG2细胞(miR-106b下调组),并设空...

Effect of miR-106b on radiosensitivity of hepatoma cells and its mechanism

Objective To investigate the effect of miR-106 b on the radiosensitivity of hepatoma cells and its possible mechanism.Methods The expression of miR-106 b in human hepatoma cell lines HepG2,SMMC-7721,SK-HEP-1,Huh7 and normal hepatocyte QSG7701 were detected by q RT-PCR.The HepG2 cells were transfected with miR-106 b siRNA(miR-106 b 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-PI3 K/PI3 K,p-AKT/AKT,PCNA and Bax were detected by Western blot.Results Compared with QSG7701 cells,the expression level of miR-106 b in HepG2,SMMC-7721,SK-HEP-1,and Huh7 cells was increased(all P<0.05),and the expression level of miR-106 b 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-PI3 K/PI3 K,p-AKT/AKT and PCNA in miR-106 b 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-106 b 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 PI3 K/AKT pathway activation.