Department of Infectious Diseases, The Second Affiliated Hospital of Shandong First Medical University, Tai'an, Shandong 271000, P.R. China.
Department of Pharmacy, Liaocheng People's Hospital, Liaocheng, Shandong 252000, P.R. China.
Mol Med Rep. 2021 May;23(5). doi: 10.3892/mmr.2021.12025. Epub 2021 Mar 24.
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 . 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.
乙型肝炎病毒（HBV）是导致肝脏相关癌症的主要原因之一。在研究乙型肝炎病毒相关肝癌中的 microRNA（miRNA 或 miR）功能方面已经取得了进展。因此，本研究旨在确定 miR-1271-5p 在乙型肝炎病毒相关肝癌中的作用和功能机制。通过逆转录-定量 PCR（RT-qPCR）测量 miR-1271-5p 和水通道蛋白 5（AQP5）在 mRNA 水平上的表达。通过 ELISA 或 qPCR 评估乙型肝炎 e-抗原（HBeAg）、乙型肝炎表面抗原（HBsAg）和 HBV DNA 的水平。通过细胞计数试剂盒-8、流式细胞术或 Transwell 测定法检测细胞活力、凋亡、迁移和侵袭。通过双荧光素酶报告基因检测和 RNA 结合蛋白免疫沉淀测定法预测 miR-1271-5p 和 AQP5 的相互作用。AQP5、Bax、Bcl-2、cleaved-caspase-3 和增殖细胞核抗原的蛋白水平通过 Western blot 分析进行量化。通过裸鼠肿瘤发生测定法检查 miR-1271-5p 的作用。miR-1271-5p 在乙型肝炎病毒相关肝癌细胞和组织中下调，而 AQP5 上调。miR-1271-5p 的过表达或 AQP5 的敲低抑制了 HBeAg、HBsAg 和 HBV DNA 的水平，阻断了细胞活力、迁移和侵袭，并诱导了凋亡。AQP5 被确认为 miR-1271-5p 的直接靶标，miR-1271-5p 通过靶向 AQP5 发挥其作用。miR-1271-5p 的过表达通过削弱 AQP5 的表达来阻碍体内肿瘤生长。总之，miR-1271-5p 通过竞争性靶向 AQP5 阻断 HBV 诱导的肝癌进展。
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