title: MiR-210 up-regulation inhibits proliferation and induces apoptosis in glioma cells by targeting SIN3A.
abstract: BACKGROUND
  The aim of this study was to determine whether miR-210 can affect the apoptosis and proliferation of human U251 glioma cells from down-regulating SIN3A.
  
  
  METHODS
  The expression of miRNA-210 was detected by quantitative real-time PCR in normal brain tissue and glioma samples. The apoptosis and proliferation ability of U251 cells were analyzed by MTT and flow cytometry assay after anti-miR-210 transfection. For the regulation mechanism analysis of miR-210, TargetScan, PicTar, and microRNA were selected to predict some potential target genes of miR-210. The predicted gene was identified to be the direct and specific target gene of miR-210 by luciferase activities assay and Western blot. RNA interference technology was used to confirm that the apoptosis and proliferation effects of miR-210 were directly induced by SIN3A.
  
  
  RESULTS
  The expression of miR-210 increased significantly in glioma in comparison with normal brain tissue. The silence of miR-210 expression could inhibit the proliferation of U251 cells and induce the apoptosis. Mechanism analysis revealed that SIN3A was a specific and direct target gene of miR-210. The siRNA-SIN3A could down-regulate the expression of SIN3A protein, which was up-regulated in U251 cells by anti-miR-210 transfection, and our experiments found that silence of SIN3A could inhibit the apoptosis and sharply increase the proliferation of U251 cells. The regulation effects of anti-miR-210 on apoptosis and proliferation can be reversed respectively by the expression silence of SIN3A.
  
  
  CONCLUSIONS
  Aberrantly expressed miR-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression. This might offer a new potential therapeutic stratagem for glioma.
authors.affiliation: Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning, China (mainland).
authors.forename: Chao
authors.initials: C
authors.lastname: Shang
authors.affiliation: Department of Neurosurgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning, China (mainland).
authors.forename: Yang
authors.initials: Y
authors.lastname: Hong
authors.affiliation: Department of Central Laboratory, School of Stomatology, China Medical University, Shenyang, Liaoning, China (mainland).
authors.forename: Yan
authors.initials: Y
authors.lastname: Guo
authors.affiliation: Department of Neurosurgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning, China (mainland).
authors.forename: Yun-hui
authors.initials: YH
authors.lastname: Liu
authors.affiliation: Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning, China (mainland).
authors.forename: Yi-xue
authors.initials: YX
authors.lastname: Xue
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D000368:Aged; D017209:Apoptosis / Q000235:genetics*; D001483:Base Sequence; D001932:Brain Neoplasms / Q000235:genetics* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000235:genetics* / Q000473:pathology*; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D008875:Middle Aged; D008969:Molecular Sequence Data; D060888:Real-Time Polymerase Chain Reaction; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D056264:Sin3 Histone Deacetylase and Corepressor Complex; D015854:Up-Regulation / Q000235:genetics*
chemical_list: D020413:3' Untranslated Regions; C543800:MIRN210 microRNA, human; D035683:MicroRNAs; D012097:Repressor Proteins; C099683:SIN3A transcription factor; D056264:Sin3 Histone Deacetylase and Corepressor Complex