MicroRNA-1271-5p alleviates the malignant development of hepatitis B virus-mediated liver cancer via binding to AQP5

Hepatitis B virus (HBV) is a leading cause of liver-related cancer. Progress has been made on the study of microRNA (miRNA or miR) function in HBV-related liver cancer. Hence, the objective of the present study was to determine the role and functional mechanism of miR-1271-5p in HBV-associated liver cancer. miR-1271-5p and aquaporin 5 (AQP5) expression at the mRNA level were measured by reverse transcription-quantitative PCR (RT-qPCR). The levels of hepatitis B e-antigen (HBeAg), hepatitis B surface antigen (HBsAg) and HBV DNA were assessed by ELISA or qPCR. Cell viability, apoptosis, migration and invasion were detected by Cell Counting Kit-8, flow cytometry or Transwell assay. The interaction of miR-1271-5p and AQP5 was predicted by TargetScan, and verified by Dual-luciferase reporter assay and RNA binding protein immunoprecipitation assay. The protein levels of AQP5, Bax, Bcl-2, cleaved-caspase-3 and proliferating cell nuclear antigen were quantified by western blot analysis. Nude mouse tumorigenicity assay was conducted to examine the role of miR-1271-5p in vivo. miR-1271-5p was downregulated, while AQP5 was upregulated in HBV-related liver cancer cells and tissues. Overexpression of miR-1271-5p or AQP5 knockdown inhibited the levels of HBeAg, HBsAg and HBV DNA, blocked cell viability, migration and invasion, and induced apoptosis. AQP5 was confirmed to be a direct target of miR-1271-5p, and miR-1271-5p exerted its role through targeting AQP5. Overexpression of miR-1271-5p impeded tumor growth in vivo by weakening the expression of AQP5. In conclusion, miR-1271-5p blocked the progression of HBV-induced liver cancer by competitively targeting AQP5.