title: Decreased miR-106a inhibits glioma cell glucose uptake and proliferation by targeting SLC2A3 in GBM.
abstract: BACKGROUND
  MiR-106a is frequently down-regulated in various types of human cancer. However the underlying mechanism of miR-106a involved in glioma remains elusive.
  
  
  METHODS
  The association of miR-106a with glioma grade and patient survival was analyzed. The biological function and target of miR-106a were determined by bioinformatic analysis and cell experiments (Western blot, luciferase reporter, cell cycle, ntracellular ATP production and glucose uptake assay). Finally, rescue expression of its target SLC2A3 was used to test the role of SLC2A3 in miR-106a-mediated cell glycolysis and proliferation.
  
  
  RESULTS
  Here we showed that miR-106a was a tumor suppressor miRNA was involved in GBM cell glucose uptake and proliferation. Decreased miR-106a in GBM tissues and conferred a poor survival of GBM patients. SLC2A3 was identified as a core target of miR-106a in GBM cells. Inhibition of SLC2A3 by miR-106a attenuated cell proliferation and inhibited glucose uptake. In addition, for each biological process we identified ontology-associated transcripts that significantly correlated with SLC2A3 expression. Finally, the expression of SLC2A3 largely abrogated miR-106a-mediated cell proliferation and glucose uptake in GBM cells.
  
  
  CONCLUSIONS
  Taken together, miR-106a and SLC2A3 could be potential therapeutic approaches for GBM.
authors.affiliation: Department of Neurosurgery, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China. chstroke@126.com.
authors.forename: Dong-Wei
authors.initials: DW
authors.lastname: Dai
authors.forename: Qiong
authors.initials: Q
authors.lastname: Lu
authors.forename: Lai-Xing
authors.initials: LX
authors.lastname: Wang
authors.forename: Wen-Yuan
authors.initials: WY
authors.lastname: Zhao
authors.forename: Yi-Qun
authors.initials: YQ
authors.lastname: Cao
authors.forename: Ya-Nan
authors.initials: YN
authors.lastname: Li
authors.forename: Guo-Sheng
authors.initials: GS
authors.lastname: Han
authors.forename: Jian-Min
authors.initials: JM
authors.lastname: Liu
authors.forename: Zhi-Jian
authors.initials: ZJ
authors.lastname: Yue
mesh_terms: D020029:Base Pairing; D001483:Base Sequence; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D016000:Cluster Analysis; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D005909:Glioblastoma / Q000235:genetics* / Q000378:metabolism* / Q000401:mortality; D005947:Glucose / Q000378:metabolism*; D051274:Glucose Transporter Type 3 / Q000235:genetics* / Q000378:metabolism; D006019:Glycolysis; D006801:Humans; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D011379:Prognosis; D034622:RNA Interference
chemical_list: D051274:Glucose Transporter Type 3; C542541:MIRN106 microRNA, human; D035683:MicroRNAs; D005947:Glucose