c-met expression is regulated by mitf in the melanocyte lineage

doi:10.1074/jbc.M513094200

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Papers In Press, published online ahead of print February 2, 2006
J. Biol. Chem, 10.1074/jbc.M513094200
Submitted on December 8, 2005
Revised on February 2, 2006
Accepted on February 2, 2006

c-met expression is regulated by mitf in the melanocyte lineage

Gaël G. McGill, Rizwan Haq, Emi K. Nishimura, and David E. Fisher

Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02115

Corresponding Author: david_fisher{at}dfci.harvard.edu

HGF/c-Met signaling is thought to be a key pathway in both melanocyte development and melanoma metastasis. Here, HGF stimulation of melanocytes was seen to upregulate c-Met expression. In an effort to decipher the mechanism by which HGF upregulates its receptor, we found that c-Met is a direct transcriptional target of Mitf. This was confirmed with chromatin immunoprecipitation experiments of the human c-Met promoter, as well as the ability of adenovirally expressed Mitf to modulate endogenous c-Met protein levels in melanocytes. Disruption of Mitf blocked HGF-dependent increases in endogenous c-Met message and protein levels, indicating that HGF regulates its own receptor levels via Mitf. Finally, dominant negative inhibition of Mitf resulted in profound resistance of melanocytes and melanoma cells to HGF-dependent matrix invasion, suggesting a physiologic role for this pathway in melanocytic development and melanoma.

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