Long noncoding RNA growth-arrest-specific transcript 5 (GAS5) has been proved to play a crucial role in cancer chemoresistance. However, the function of GAS5 and its underlying molecular mechanism in hepatocellular carcinoma (HCC) chemoresistance remain unknown. In this study, we aimed to investigate its function and underlying molecular mechanism in HCC cisplatin (CDDP) resistance. The results demonstrated that GAS5 was significantly downregulated in HCC tissues and cells, especially in CDDP-resistant HCC tissues and cells. Low GAS5 expression was tightly correlated with shorter survival in patients with HCC. Functionally, GAS5 overexpression sensitized CDDP-resistant HepG2/CDDP and Huh7/CDDP cells to CDDP. Mechanically, GAS5 improved the sensitivity of HCC cells to CDDP through sponging miR-222. Taken together, these observations suggested that overexpression of GAS5 overcame CDDP resistance of HCC cells by regulating miR-222, providing a potential therapeutic target for overcoming the chemoresistance of HCC cells.
Keywords: cisplatin; growth-arrest-specific transcript 5; hepatocellular carcinoma; miR-222.