A SUMOylation-Dependent Transcriptional Subprogram Is Required for Myc-Driven Tumorigenesis
Abstract
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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jan 20, 2012
- Source ID
- 10.1126/science.1212728
Entities
People
- Anthony C. Liang
- Bing Yu
- C. Kent Osborne
- Chad A. Shaw
- Chad J Creighton
- Earlene M. Schmitt
- Ido Golding
- Jessica D. Kessler
- Ji Luo
- Kristen L. Meerbrey
- Kristopher T. Kahle
- Mamie Z Li
- Michael R. Schlabach
- Mitchell Rao
- Nicole L. Solimini
- Peng Yu
- Qikai Xu
- Rachel Schiff
- Rocio Dominguez-vidana
- Ronald J. Bernardi
- Samuel O. Skinner
- Stephen Elledge
- Susan Hilsenbeck
- Thomas F. Westbrook
- Tiffany Hsu
- Tingting Sun
- Zachary C Hartman
Organizations
- Baylor College of Medicine
- Harvard Medical School
- Massachusetts General Hospital
- National Cancer Institute
- National Institutes of Health
- The University of Texas MD Anderson Cancer Center
- United States Department of Defense
- University of Illinois Urbana–Champaign