Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 277, Issue 22, Pages 19998-20010Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M200860200
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- NCI NIH HHS [CA78257] Funding Source: Medline
- NHLBI NIH HHS [HL33741] Funding Source: Medline
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Using cDNA microarrays, we recently identified a large number of transcripts that are regulated differentially by the c-Myc oncoprotein in myeloid cells. Here, we characterize one of these, termed MT-MC1 (Myc Target in Myeloid Cells-1). MT-MC1 is a widely expressed nuclear protein whose overexpression, unlike that of c-Myc targets reported previously, recapitulates multiple c-Myc phenotypes. These include promotion of apoptosis, alteration of morphology, enhancement of anchorage-independent growth, tumorigenic conversion, promotion of genomic instability, and inhibition of hematopoietic differentiation. The MT-MC1 promoter is a direct c-Myc target; it contains two consensus E-box elements, both of which bind c-Myc(.)Max heterodimers. Mutation of either site abrogates DNA binding by c-Myc-Max and renders the promoter c-Myc unresponsive. Finally, MT-MC1 regulates the expression of several other c-Myc target genes. MT-MC1 represents a proximal and direct c-Myc target that recapitulates many of the properties typically associated with Myc oneoprotein overexpression.
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