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Title 

MicroRNA miR-199a regulates the MET proto-oncogene and the downstream extracellular signal-regulated kinase 2 (ERK2)

Authors 

S KimU J LeeM N KimE J LeeJ Y KimM Y LeeS ChoungYoung Joo KimY C Choi

Publisher 

American Society for Biochemistry and Molecular Biology

Issue Date 

2008

Citation 

Journal of Biological Chemistry, vol. 283, no. 26, pp. 18158-18166

Keywords 

extracellular signalsmethylation patternsmimeticsregulated kinasesmicroRNAmitogen activated protein kinase 1DNA methylationmetabolismDNA MethylationmicroRNAs

Abstract 

MicroRNAs (miRNAs) constitute a class of small noncoding RNAs that play important roles in a variety of biological processes including development, apoptosis, proliferation, and differentiation. Here we show that the expression of miR-199a and miR-199a* (miR-199a/a*), which are processed from the same precursor, is confined to fibroblast cells among cultured cell lines. The fibroblast-specific expression pattern correlated well with methylation patterns: gene loci on chromosome 1 and 19 were fully methylated in all examined cell lines but unmethylated in fibroblasts. Transfection of miR-199a and/or -199a* mimetics into several cancer cell lines caused prominent apoptosis with miR-199a* being more pro-apoptotic. The mechanism underlying apoptosis induced by miR-199a was caspase-dependent, whereas a caspase-independent pathway was involved in apoptosis induced by miR-199a* in A549 cells. By employing microarray and immunoblotting analyses, we identified the MET proto-oncogene as a target of miR-199a*. Studies with a luciferase reporter fused to the 3′-untranslated region of the MET gene demonstrated miR-199a*-mediated down-regulation of luciferase activity through a binding site of miR-199a*. Interestingly, extracellular signal-regulated kinase 2 (ERK2) was also down-regulated by miR-199a*. Coordinated down-regulation of both MET and its downstream effector ERK2 by miR-199a* may be effective in inhibiting not only cell proliferation but also motility and invasive capabilities of tumor cells.

ISSN 

0021-9258

Link 

http://dx.doi.org/10.1074/jbc.M800186200

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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