Metastasis-associated protein 1 (MTA1) is an essential downstream effector of the c-MYC oncoprotein.
The c-myc oncogene is among the most commonly overexpressed genes in human cancer. c-myc encodes a basic helix-loop-helix/ leucine zipper (bHLH/LZ) transcription factor (c-MYC) that activates a cascade of downstream targets that ultimately mediate cellular transformation. Although a large number of genes are regulated by c-MYC, only a few have been functionally linked to c-MYC-mediated transformation. By expression profiling, the metastasis-associated protein 1 (MTA1) gene was identified here as a target of the c-MYC oncoprotein in primary human cells, a result confirmed in human cancer cells. MTA1 itself has been previously implicated in cellular transformation, in part through its ability to regulate the epithelial-to-mesenchymal transition and metastasis. MTA1 is a component of the Mi-2/nucleosome remodeling and deacetylating (NURD) complex that contains both histone deacetylase and nucleosome remodeling activity. The data reported here demonstrate that endogenous c-MYC binds to the genomic MTA1 locus and recruits transcriptional coactivators. Most importantly, short hairpin RNA (shRNA)-mediated knockdown of MTA1 blocks the ability of c-MYC to transform mammalian cells. These data implicate MTA1 and the Mi-2/NURD complex as one of the first downstream targets of c-MYC function that are essential for the transformation potential of c-MYC.[1]References
- Metastasis-associated protein 1 (MTA1) is an essential downstream effector of the c-MYC oncoprotein. Zhang, X.Y., DeSalle, L.M., Patel, J.H., Capobianco, A.J., Yu, D., Thomas-Tikhonenko, A., McMahon, S.B. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
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