title: [miR-216b suppresses cell proliferation and invasion by targeting PKCα in nasopharyngeal carcinoma cells].
abstract: OBJECTIVE
  To elucidate whether miR-216b suppresses cell proliferation and invasion by targeting PKCα, thus to reveal the molecular mechanism that miR-216b functions as a tumor suppressor in nasopharyngeal carcinoma (NPC).
  
  
  METHODS
  PKCα 3'UTR-luciferase vector was constructed and dual-luciferase reporter gene assay was employed to examine the effect of miR-216b on luciferase activity. Nasopharyngeal cancer CNE2 cells were transfected with miR-216b mimics, and then qRT-PCR and Western blotting were performed to detect the expressions of PKCa mRNA and protein. The effects of PKCα downregulation on cell proliferation and invasion were assessed after PKCα siRNA were transfected into CNE2 cells. CNE2 cells were cotransfected with miR-216b mimics and PKCα plasmid, and the proliferation of CNE2 cells was assayed using a MTS cell proliferation assay kit.
  
  
  RESULTS
  The results of dual-luciferase reporter gene assay demonstrated that miR-216b could bind to the 3'-untranslated region (UTR) of PKCα and inhibited the luciferase activity to 62.4% of that of the mimics control cells. The expressions of PKCα mRNA and protein were significantly down-regulated by 49.1% and 55.7%, respectively, in comparison with that of the control cells. siRNA-mediated downregulation of PKCα suppressed the proliferation and invasion ability of CNE2 cells, and could partially mimic the tumor-inhibiting effect of miR-216b. Moreover, the overexpressed PKCα may partially reverse the inhibitory effect of miR-216b on proliferation of CNE2 cells.
  
  
  CONCLUSIONS
  miR-216b suppresses cell proliferation and invasion by targeting PKCα in NPC cells.
authors: Cancer Hospital and Cancer Research Institute, Guangzhou Medical University, Guangzhou 510095, China.
authors: Min
authors: M
authors: Deng
authors: Cancer Hospital and Cancer Research Institute, Guangzhou Medical University, Guangzhou 510095, China.
authors: Ji-fang
authors: JF
authors: Liu
authors: Cancer Hospital and Cancer Research Institute, Guangzhou Medical University, Guangzhou 510095, China.
authors: Yi-xue
authors: YX
authors: Gu
authors: Cancer Hospital and Cancer Research Institute, Guangzhou Medical University, Guangzhou 510095, China.
authors: Guo-pei
authors: GP
authors: Zheng
authors: Cancer Hospital and Cancer Research Institute, Guangzhou Medical University, Guangzhou 510095, China. Email: hezhimin2005@yahoo.com.
authors: Zhi-min
authors: ZM
authors: He
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D005822:Genetic Vectors; D006801:Humans; D008156:Luciferases / Q000235:genetics; D035683:MicroRNAs / Q000235:genetics*; D009303:Nasopharyngeal Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D009361:Neoplasm Invasiveness; D010957:Plasmids; D051571:Protein Kinase C-alpha / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D014162:Transfection
chemical_list: D020413:3' Untranslated Regions; C575482:MIRN216 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D008156:Luciferases; D051571:Protein Kinase C-alpha