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SNIP1 is a candidate modifier of the transcriptional activity of c-Myc on E box-dependent target genes.

Fujii M, Lyakh LA, Bracken CP, Fukuoka J, Hayakawa M, Tsukiyama T, Soll SJ, Harris M, Rocha S, Roche KC, Tominaga S, Jen J, Perkins ND, Lechleider RJ, Roberts AB

Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892, USA.

Using a yeast two-hybrid screen, we found that SNIP1 (Smad nuclear-interacting protein 1) associates with c-Myc, a key regulator of cell proliferation and transformation. We demonstrate that SNIP1 functions as an important regulator of c-Myc activity, binding the N terminus of c-Myc through its own C terminus, and that SNIP1 enhances the transcriptional activity of c-Myc both by stabilizing it against proteosomal degradation and by bridging the c-Myc/p300 complex. These effects of SNIP1 on c-Myc likely contribute to synergistic effects of SNIP1, c-Myc, and H-Ras in inducing formation of foci in an in vitro transformation assay and also in supporting anchorage-independent growth. The significant association of SNIP1 and c-Myc staining in a non-small cell lung cancer tissue array is further evidence that their activities might be linked and suggests that SNIP1 might be an important modulator of c-Myc activity in carcinogenesis.

Published 12 December 2006 in Mol Cell, 24(5): 771-83.
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