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Emerging evidence has unveiled that miR\u2010139\u20105p is aberrantly downregulated in cancers, including\n GBC<\/jats:styled-content>\n . However, the functions and mechanisms of miR\u2010139\u20105p in\n GBC<\/jats:styled-content>\n remain unclear.\n <\/jats:p>\n <\/jats:sec>\n \n Materials and methods<\/jats:title>\n \n MiR\u2010139\u20105p\u2010overexpression was established in\n GBC cell<\/jats:styled-content>\n lines, after which cell proliferation, migration, invasion, colony formation, and glucose metabolism were assayed in vitro. Subsequently, bioinformatics prediction and dual\u2010luciferase reporter were performed to confirm that pyruvate kinase M2 (\n PKM<\/jats:styled-content>\n 2) was a direct target of mi\n RNA<\/jats:styled-content>\n \u2010139\u20105p. Xenograft mouse models were applied to investigate the role of miR\u2010139\u20105p in\n GBC<\/jats:styled-content>\n tumourigenicity in vivo. In situ hybridization and immunohistochemical assays were performed to determine the relationships among miR\u2010139\u20105p,\n PKM<\/jats:styled-content>\n 2 expression and clinical malignancies in\n GBC<\/jats:styled-content>\n samples.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n We found that miR\u2010139\u20105p was substantially downregulated in\n GBC<\/jats:styled-content>\n tissues. Low expression of miR\u2010139\u20105p was significantly associated with poor clinical outcomes.\n GBC cell<\/jats:styled-content>\n proliferation, migration, and invasion could be inhibited by overexpression of miR\u2010139\u20105p either in vitro or in vivo. In addition, miR\u2010139\u20105p overexpression could directly inhibit\n PKM<\/jats:styled-content>\n 2 expression and lead to suppression of glucose consumption, lactate production, and cellular\n ATP<\/jats:styled-content>\n levels. Moreover,\n PKM<\/jats:styled-content>\n 2 was frequently upregulated in\n GBC<\/jats:styled-content>\n and correlated with poor prognosis. Mechanistically, mi\n RNA<\/jats:styled-content>\n \u2010139\u20105p inhibited cell proliferation, migration, and glycolysis in\n GBC<\/jats:styled-content>\n , at least in part, by repressing\n PKM<\/jats:styled-content>\n 2.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n These results demonstrated a novel role for miR\u2010139\u20105p\/\n PKM<\/jats:styled-content>\n 2 in\n GBC<\/jats:styled-content>\n progression and provided potential prognostic predictors for\n GBC<\/jats:styled-content>\n patients.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/cpr.12510","type":"journal-article","created":{"date-parts":[[2018,8,14]],"date-time":"2018-08-14T02:50:31Z","timestamp":1534215031000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["MiR\u2010139\u20105p is associated with poor prognosis and regulates glycolysis by repressing\n PKM<\/scp>\n 2 in gallbladder carcinoma"],"prefix":"10.1111","volume":"51","author":[{"given":"Jianan","family":"Chen","sequence":"first","affiliation":[{"name":"Precision Medicine Center The First Affiliated Hospital of Zhengzhou University Zhengzhou China"},{"name":"Key Laboratory of Clinical Medicine The First Affiliated Hospital of Zhengzhou University Zhengzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Yu","sequence":"additional","affiliation":[{"name":"Precision Medicine Center The First Affiliated Hospital of Zhengzhou University Zhengzhou China"},{"name":"Key Laboratory of Clinical Medicine The First Affiliated Hospital of Zhengzhou University Zhengzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaolong","family":"Chen","sequence":"additional","affiliation":[{"name":"Precision Medicine Center The First Affiliated Hospital of Zhengzhou University Zhengzhou China"},{"name":"Key Laboratory of Clinical Medicine The First Affiliated 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