biostudies-literatureJin HNatural Science Foundation of ChinaWenzhou Science and Technology BureauWenzhou Medical UniversityStartup Foundation for Hundred-Talent Program of Zhejiang UniversityKey Discipline of Zhejiang Province in Medical TechnologyKey Project of Science and Technology Innovation Team of Zhejiang ProvinceNational Natural Science Foundation of China840-854https://www.ebi.ac.uk/biostudies/studies/S-EPMC8078721biostudies-literatureUnknown17(4)Although <i>MIR516A</i> has been reported to be downregulated and act as a tumor suppressor in multiple cancers, its expression and potential contribution to human bladder cancer (BC) remain unexplored. Unexpectedly, we showed here that <i>MIR516A</i> was markedly upregulated in human BC tissues and cell lines, while inhibition of <i>MIR516A</i> expression attenuated BC cell monolayer growth <i>in vitro</i> and xenograft tumor growth <i>in vivo</i>, accompanied with increased expression of PHLPP2. Further studies showed that <i>MIR516A</i> was able to directly bind to the 3'-untranslated region of <i>PHLPP2</i> mRNA, which was essential for its attenuating PHLPP2 expression. The knockdown of <i>PHLPP2</i> expression in <i>MIR516A</i>-inhibited cells could reverse BC cell growth, suggestingAutophagyOncogenic role of <i>MIR516A</i> in human bladder cancer was mediated by its attenuating PHLPP2 expression and BECN1-dependent autophagy.PMC8078721First ClassCategory A2013TD10Y201700282017R413064Y20190065NSFC81702530NSFC8187258789216021Li HHuang CLiu LLu YHuang HChen CXie QChang YXu JZang NTian ZZhao NJin HFang ZHuang XMa JWang XfalseOncogenic role of <i>MIR516A</i> in human bladder cancer was mediated by its attenuating PHLPP2 expression and BECN1-dependent autophagy.Although <i>MIR516A</i> has been reported to be downregulated and act as a tumor suppressor in multiple cancers, its expression and potential contribution to human bladder cancer (BC) remain unexplored. Unexpectedly, we showed here that <i>MIR516A</i> was markedly upregulated in human BC tissues and cell lines, while inhibition of <i>MIR516A</i> expression attenuated BC cell monolayer growth <i>in vitro</i> and xenograft tumor growth <i>in vivo</i>, accompanied with increased expression of PHLPP2. Further studies showed that <i>MIR516A</i> was able to directly bind to the 3'-untranslated region of <i>PHLPP2</i> mRNA, which was essential for its attenuating PHLPP2 expression. The knockdown of <i>PHLPP2</i> expression in <i>MIR516A</i>-inhibited cells could reverse BC cell growth, suggesting2021-01-01T00:00:00Z2021 Apr2026-07-09T11:33:30.116Z2026-07-09T10:50:51.077ZS-EPMC80787213211610910.1080/15548627.2020.1733262