PUBLICATION

MiR-150 negatively regulates c-Myb expression, which is evolutionarily conserved and plays an important role in developmental process

Authors
Lin, Y.C., Kuo, M.W., Yu, J., Kuo, H.H., Lin, R.J., Lo, W.L., and Yu, A.L.
ID
ZDB-PUB-080801-18
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.
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.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping