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ZIRC
ZFIN ID: ZDB-PUB-080801-18
MiR-150 negatively regulates c-Myb expression, which is evolutionarily conserved and plays an important role in developmental process
Lin, Y.C., Kuo, M.W., Yu, J., Kuo, H.H., Lin, R.J., Lo, W.L., and Yu, A.L.
Date: 2008
Source: Mol. Biol. Evol.   25(10): 2189-2198 (Journal)
Registered Authors:
Keywords: microRNA, miR-150, c-Myb
MeSH Terms:
  • 3' Untranslated Regions
  • Animals
  • Base Sequence
  • Cell Line, Tumor
  • Chromosome Aberrations
  • Evolution, Molecular*
  • Gene Expression Regulation, Developmental*
  • Humans
  • Lymphocytes/metabolism
  • Mice
  • MicroRNAs/metabolism*
  • Molecular Sequence Data
  • Phenotype
  • Proto-Oncogene Proteins c-myb/genetics*
  • Proto-Oncogene Proteins c-myb/metabolism*
  • Zebrafish
PubMed: 18667440 Full text @ Mol. Biol. Evol.
FIGURES
ABSTRACT
Human c-Myb proto-oncogene is highly expressed in hematopoietic progenitors as well as leukemia and certain solid tumor. However, the regulatory mechanisms of its expression and biological functions remain largely unclear. Recently, c-Myb has been shown to be targeted by microRNA-150 (miR-150) which thereby controls B cell differentiation in mice. In this study, we demonstrated that c-Myb is an evolutionarily conserved target of miR-150 in human and zebrafish, using reporter assays. Ectopic expression of miR-150 in breast cancer and leukemic cells repressed endogenous c-Myb at both mRNA and protein levels. Among several leukemia cell lines, primary leukemia cells, and normal lymphocytes, expression levels of miR-150 inversely correlated with c-Myb. MiR-150 over-expression or c-Myb silencing in zebrafish zygotes led to similar and serious phenotypic defects in zebrafish, and the phenotypic aberrations induced by miR-150 could be reversed by co-injection of c-Myb mRNA. Our findings suggest that c-Myb is an evolutionally conserved target of miR-150 and miR-150/c-Myb interaction is important for embryonic development and possibly oncogenesis.
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