Editors' ChoiceCancer

Taking the Myc

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Science Signaling  24 Jan 2012:
Vol. 5, Issue 208, pp. ec29
DOI: 10.1126/scisignal.2002877

Despite nearly 30 years of research into the mechanisms by which Myc oncogene dysregulation contributes to tumorigenesis, there are still no effective therapies that inhibit Myc activity. Kessler et al. (see the Perspective by Evan) searched for gene products that support Myc-driven tumorigenesis. One pharmacologically tractable target that emerged from the screen was the SUMO-activating enzyme complex SAE1/2, which catalyzes a posttranslational modification (SUMOylation) that alters protein behavior and function. SUMOylation was found to control the Myc transcriptional response, and its inhibition caused mitotic defects and apoptosis in Myc-dependent breast cancer cells.

J. D. Kessler, K. T. Kahle, T. Sun, K. L. Meerbrey, M. R. Schlabach, E. M. Schmitt, S. O. Skinner, Q. Xu, M. Z. Li, Z. C. Hartman, M. Rao, P. Yu, R. Dominguez-Vidana, A. C. Liang, N. L. Solimini, R. J. Bernardi, B. Yu, T. Hsu, I. Golding, J. Luo, C. K. Osborne, C. J. Creighton, S. G. Hilsenbeck, R. Schiff, C. A. Shaw, S. J. Elledge, T. F. Westbrook, A SUMOylation-dependent transcriptional subprogram is required for Myc-driven tumorigenesis. Science 335, 348–353 (2012). [Abstract] [Full Text]

G. Evan, Taking a back door to target Myc. Science 335, 293–294 (2012). [Abstract] [Full Text]

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