Abstract
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.