Report

A SUMOylation-Dependent Transcriptional Subprogram Is Required for Myc-Driven Tumorigenesis

See allHide authors and affiliations

Science  20 Jan 2012:
Vol. 335, Issue 6066, pp. 348-353
DOI: 10.1126/science.1212728

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Taking the Myc

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. (p. 348, published online 8 December; 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.

View Full Text