{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T03:02:33Z","timestamp":1771297353274,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,12,4]],"date-time":"2018-12-04T00:00:00Z","timestamp":1543881600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hepatocellular carcinoma (HCC) is mainly associated with hepatitis B virus (HBV) infection and characterized by metastasizing and infiltrating adjacent and distant tissues. Notably, microRNA\u20101271 (miR\u20101271) is a tumor suppressor in various cancers. Therefore, we evaluate the ability of miR\u20101271 to influence cell proliferation, migration, invasion, and apoptosis in HBV\u2010associated HCC through the Adenosine monophosphate\u2013activated protein kinase (AMPK) signaling pathway via targeting <jats:italic>CCNA1<\/jats:italic>. HBV\u2010associated HCC and adjacent normal tissues were collected to identify the expression of miR\u20101271 and CCNA1. To verify the relationship between miR\u20101271 and <jats:italic>CCNA1<\/jats:italic>, we used bioinformatics prediction and the dual\u2010luciferase reporter gene assay. The effects of miR\u20101271 on HBV\u2010associated HCC cell behaviors were investigated by treatment of the miR\u20101271 mimic, the miR\u20101271 inhibitor, or small interfering RNA\u00a0against CCNA1. The HBV\u2010DNA quantitative assay, 3\u2010(4,5\u2010dimethylthiazol\u20102\u2010yl)\u20102,5\u2010diphenyltetrazolium bromid assay, scratch test, transwell assay, and flow cytometry were used to detect HBV\u2010DNA replication, cell proliferation, invasion, migration, and apoptosis. MiR\u20101271 showed a low expression, whereas CCNA1 showed a high expression in HBV\u2010associated HCC tissues. We identified that miR\u20101271 targeted and negatively regulated <jats:italic>CCNA1<\/jats:italic>. Upregulated miR\u20101271 and downregulated CCNA1 inhibited the HBV\u2010associated HCC cell HBV\u2010DNA replication, proliferation, migration, and invasion, while accelerating apoptosis by activating the AMPK signaling pathway. MiR\u20101271 promotes the activation of the AMPK signaling pathway by binding to <jats:italic>CCNA1<\/jats:italic>, whereby miR\u20101271 suppresses HBV\u2010associated HCC progression. This study points to a potential therapeutic approach of downregulation of miR\u20101271 in HBV\u2010associated HCC treatment.<\/jats:p>","DOI":"10.1002\/jcp.26955","type":"journal-article","created":{"date-parts":[[2018,12,19]],"date-time":"2018-12-19T15:08:50Z","timestamp":1545232130000},"page":"3555-3569","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["<i>Retracted<\/i>: MicroRNA\u20101271 functions as a potential tumor suppressor in hepatitis B virus\u2013associated hepatocellular carcinoma through the AMPK signaling pathway by binding to <i>CCNA1<\/i>"],"prefix":"10.1002","volume":"234","author":[{"given":"Yang","family":"Chen","sequence":"first","affiliation":[{"name":"Department of General Surgery The Seventh Affiliated Hospital of Sun Yat\u2010sen University Shenzhen 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