title: MiR-125b expression affects the proliferation and apoptosis of human glioma cells by targeting Bmf.
abstract: BACKGROUND
  MicroRNAs (miRNAs) are small noncoding RNAs whose function as modulators of gene expression is crucial for the proper control of cell growth. Although many microRNAs were found to express in central nervous system (CNS), the role of the regulatory networks in which they are involved and their function in the pathological process of nerve cells are only just emerging. In the present study, the possible mechanisms by which one neuronal miRNAs, miR-125b, affected the growth of nervous cells were investigated using in vitro cell line model.
  
  
  METHODS
  The expression pattern of miR-125b in ATRA-treated human glioma cell lines was detected by Northern blotting and in situ localization. The effect of miR-125b on the proliferation and apoptosis of human glioma cells was analyzed by MTS assay, TUNEL and Flow cytometry analysis. In addition, the identification of target gene of miR-125b was studied by dual-luciferase activity assay and Immunoblot Analysis.
  
  
  RESULTS
  We found differential expression of miR-125b in 1.0 microM all-trans-retinoic acid (ATRA)-treated human glioma cell lines. Up-regulation of miR-125b partially restored cell viability and inhibited cell apoptosis in U343 cells treated by ATRA. Down-regulation of miR-125b decreased human glioma cells proliferation and enhanced the sensitivity of human glioma cells to ATRA-induced apoptosis. In addition, we found an inverse relationship between the expression of miR-125b and the cell apoptosis-related protein Bcl-2 modifying factor (Bmf), and miR-125b can interact with 3'-untranslated region (UTR) of Bmf.
  
  
  CONCLUSIONS
  These findings indicate that overexpression of miR-125b promotes human glioma cell proliferation and inhibits ATRA-induced cell apoptosis and low expression of miR-125b sensitizes cells to ATRA-induced apoptosis. BMF may play an important role in the process of miR-125b influencing cell apoptosis.
authors.affiliation: Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing, China.
authors.forename: Hong-Fei
authors.initials: HF
authors.lastname: Xia
authors.forename: Tian-Zhu
authors.initials: TZ
authors.lastname: He
authors.forename: Chun-Mei
authors.initials: CM
authors.lastname: Liu
authors.forename: Yi
authors.initials: Y
authors.lastname: Cui
authors.forename: Pei-Pei
authors.initials: PP
authors.lastname: Song
authors.forename: Xiao-Hua
authors.initials: XH
authors.lastname: Jin
authors.forename: Xu
authors.initials: X
authors.lastname: Ma
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism*; D017209:Apoptosis; D001483:Base Sequence; D049109:Cell Proliferation; D015536:Down-Regulation; D005910:Glioma / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C486655:BMF protein, human; C531888:MIRN125 microRNA, human; D035683:MicroRNAs; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D014212:Tretinoin