c-Myb is an evolutionary conserved miR-150 target and miR-150/c-Myb interaction is important for embryonic development.

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 evolutionary 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 messenger RNA (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. The miR-150 overexpression 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 coinjection 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.

journal_name

Mol Biol Evol

authors

Lin YC,Kuo MW,Yu J,Kuo HH,Lin RJ,Lo WL,Yu AL

doi

10.1093/molbev/msn165

subject

Has Abstract

pub_date

2008-10-01 00:00:00

pages

2189-98

issue

10

eissn

0737-4038

issn

1537-1719

pii

msn165

journal_volume

25

pub_type

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