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Oncogene DOI:10.1038/onc.2013.543

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

Publication TypeJournal Article
Year of Publication2015
AuthorsShen, RR, Zhou, AY, Kim, E, O'Connell, JT, Hagerstrand, D, Beroukhim, R, Hahn, WC
Date Published2015 Jan 08
KeywordsAnimals, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, HEK293 Cells, Heterografts, Humans, MCF-7 Cells, Mice, Inbred BALB C, Mice, Nude, Neoplasms, NF-kappa B, Oncogenes, Phosphorylation, Signal Transduction, TNF Receptor-Associated Factor 2

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.


Alternate JournalOncogene
PubMed ID24362534
PubMed Central IDPMC4067463
Grant ListF32 CA128265 / CA / NCI NIH HHS / United States
P01 CA154303 / CA / NCI NIH HHS / United States
P30 CA006516 / CA / NCI NIH HHS / United States
R01 CA130988 / CA / NCI NIH HHS / United States