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Oncogene. 2015 Jan 8;34(2):209-16. doi: 10.1038/onc.2013.543. Epub 2013 Dec 23.

TRAF2 is an NF-κB-activating oncogene in epithelial cancers.

Author information

1
1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA [3] Broad Institute of Harvard and MIT, Cambridge, MA, USA.

Abstract

Aberrant nuclear factor (NF)-κB activation is frequently observed in human cancers. Genome characterization efforts have identified genetic alterations in multiple components of the NF-κB pathway, some of which have been shown to be essential for cancer initiation and tumor maintenance. Here, using patient tumors and cancer cell lines, we identify the NF-κB regulator, TRAF2 (tumor necrosis factor (TNF) receptor-associated factor 2), as an oncogene that is recurrently amplified and rearranged in 15% of human epithelial cancers. Suppression of TRAF2 in cancer cells harboring TRAF2 copy number gain inhibits proliferation, NF-κB activation, anchorage-independent growth and tumorigenesis. Cancer cells that are dependent on TRAF2 also require NF-κB for survival. The phosphorylation of TRAF2 at serine 11 is essential for the survival of cancer cells harboring TRAF2 amplification. Together, these observations identify TRAF2 as a frequently amplified oncogene.

PMID:
24362534
PMCID:
PMC4067463
DOI:
10.1038/onc.2013.543
[Indexed for MEDLINE]
Free PMC Article

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