A SUMOylation-Dependent Transcriptional Subprogram Is Required for Myc-Driven Tumorigenesis
Copyright policy )A SUMOylation-Dependent Transcriptional Subprogram Is Required for Myc-Driven Tumorigenesis
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.
- University of Illinois System United States
- Massachusetts General Hospital United States
- National Cancer Institute United States
- Howard Hughes Medical Institute United States
- The University of Texas System United States
Gene Expression Profiling, Cell Cycle, Genes, myc, Mammary Neoplasms, Experimental, Mice, Nude, Mitosis, Sumoylation, Breast Neoplasms, Spindle Apparatus, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Mice, Cell Transformation, Neoplastic, Cell Line, Tumor, Animals, Humans, Female, RNA Interference, RNA, Small Interfering, Neoplasm Transplantation
Gene Expression Profiling, Cell Cycle, Genes, myc, Mammary Neoplasms, Experimental, Mice, Nude, Mitosis, Sumoylation, Breast Neoplasms, Spindle Apparatus, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Mice, Cell Transformation, Neoplastic, Cell Line, Tumor, Animals, Humans, Female, RNA Interference, RNA, Small Interfering, Neoplasm Transplantation
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