The function of miR-27b on the chemoresistance of hepatocellular carcinoma

Abstract

Abstract The chemoresistance of hepatocellular carcinoma (HCC) is associated with certain microRNA level. Specifically, previous studies have found that miR-27b expression is upregulated in all four HCC drug-resistance cell lines. Despite that, the function of miR-27b in HCC is not clear yet. The purpose of this study was to investigate the effect of miR-27b on chemotherapy resistance in a model of HCC. To establish stable overexpression of miR-27b and negative control HCC cell lines, a lentiviral pre-miR-27b overexpression vector and negative control vector were transfected into each cell line. The expression of miR-27b was detected with quantitative real-time PCR. CCK-8 assay, clone formation assay and immunohistochemical assay were used to detect cell proliferation. Apoptosis and drug sensitivity were detected by flow cytometry and MTT assay, respectively. The level of miR-27b in five HCC cell lines (Huh-7, HepG2, SK-Hep1 and MHCC97h, SMMC7721) was lower than that of in the normal liver cell line LO2. miR-27b level in HCC tissues was also lower than in liver tissues adjacent to the tumor. Two stable miR-27b overexpression HCC cell lines (Huh-7/miR-27b and HepG2/miR-27b) and their control cell lines (Huh-7/NC and HepG2/NC) were successfully constructed. We found that upregulation of miR-27b can reduced chemosensitivity of HCC cell to 5-FU, ADR and CDDP. Simultaneously, miR-27b promote cell apoptosis and suppress cell proliferation. Our study suggests that miR-27b acts as a biomarker to estimate drug sensitivity to chemotherapy in HCC patients. In addition, miR-27b functions as an HCC suppressor.