Taking a Back Door to Target Myc

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Science  20 Jan 2012:
Vol. 335, Issue 6066, pp. 293-294
DOI: 10.1126/science.1217819

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The transcription factor Myc coordinates the expression of a vast and functionally diverse repertoire of thousands of genes that, together, are required for the orderly proliferation of somatic cells within the body. These include genes that govern processes within the cell, such as the cell division cycle, cell metabolism and biosynthesis, cell architecture, and cell survival, as well as the multitude of processes that proliferating cells need to engage in their surrounding microenvironment, such as the generation of blood vessels, tissue remodeling, and the recruitment of cells loaded with enzymes and growth factors needed to do this. Myc is functionally nonredundant and absolutely required for the efficient proliferation of normal and cancer cells. Its expression depends on growth signals in normal cells, ensuring that its growth-promoting activities are unleashed only in cells instructed to proliferate. Control of Myc expression in cancer cells is almost always compromised. Mutations that cause Myc to become hyperactived cause uncontrollable cell proliferation and tumor formation. However, Myc has proven to be an elusive target for drug development. On page 348 of this issue, Kessler et al. (1) provide insight into how Myc's oncogenic activity might be suppressed by targeting nononcogenic proteins whose functions help Myc to transform cells.