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

Oncogene
Authors
Keywords
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.

Year of Publication
2015
Journal
Oncogene
Volume
34
Issue
2
Pages
209-16
Date Published
2015 Jan 08
ISSN
1476-5594
URL
DOI
10.1038/onc.2013.543
PubMed ID
24362534
PubMed Central ID
PMC4067463
Links
Grant list
F32 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