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Retracted : MicroRNA‐1271 functions as a potential tumor suppressor in hepatitis B virus–associated hepatocellular carcinoma through the AMPK signaling pathway by binding to CCNA1
Author(s) -
Chen Yang,
Zhao ZhenXian,
Huang Fei,
Yuan XiaoWei,
Deng Liang,
Tang Di
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26955
Subject(s) - hepatitis b virus , cell cycle , cancer research , microrna , apoptosis , flow cytometry , cell growth , chemistry , microbiology and biotechnology , biology , virology , virus , gene , biochemistry
Hepatocellular carcinoma (HCC) is mainly associated with hepatitis B virus (HBV) infection and characterized by metastasizing and infiltrating adjacent and distant tissues. Notably, microRNA‐1271 (miR‐1271) is a tumor suppressor in various cancers. Therefore, we evaluate the ability of miR‐1271 to influence cell proliferation, migration, invasion, and apoptosis in HBV‐associated HCC through the Adenosine monophosphate–activated protein kinase (AMPK) signaling pathway via targeting CCNA1 . HBV‐associated HCC and adjacent normal tissues were collected to identify the expression of miR‐1271 and CCNA1. To verify the relationship between miR‐1271 and CCNA1 , we used bioinformatics prediction and the dual‐luciferase reporter gene assay. The effects of miR‐1271 on HBV‐associated HCC cell behaviors were investigated by treatment of the miR‐1271 mimic, the miR‐1271 inhibitor, or small interfering RNA against CCNA1. The HBV‐DNA quantitative assay, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromid assay, scratch test, transwell assay, and flow cytometry were used to detect HBV‐DNA replication, cell proliferation, invasion, migration, and apoptosis. MiR‐1271 showed a low expression, whereas CCNA1 showed a high expression in HBV‐associated HCC tissues. We identified that miR‐1271 targeted and negatively regulated CCNA1 . Upregulated miR‐1271 and downregulated CCNA1 inhibited the HBV‐associated HCC cell HBV‐DNA replication, proliferation, migration, and invasion, while accelerating apoptosis by activating the AMPK signaling pathway. MiR‐1271 promotes the activation of the AMPK signaling pathway by binding to CCNA1 , whereby miR‐1271 suppresses HBV‐associated HCC progression. This study points to a potential therapeutic approach of downregulation of miR‐1271 in HBV‐associated HCC treatment.