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

R R Shen1, A Y Zhou1, E Kim1

  • 11] 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.

Oncogene
|December 24, 2013
PubMed

Insights

Tumor necrosis factor receptor-associated factor 2 (TRAF2) acts as an oncogene amplified in 15% of epithelial cancers. Inhibiting TRAF2 halts cancer cell growth and survival, highlighting its role in tumorigenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Aberrant nuclear factor (NF)-κB activation is a hallmark of human cancers.
  • Genetic alterations in NF-κB pathway components are crucial for cancer initiation and progression.

Purpose of the Study:

  • To identify novel oncogenes within the NF-κB pathway.
  • To investigate the role of tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2) in human epithelial cancers.

Main Methods:

  • Analysis of patient tumors and cancer cell lines for genetic alterations.
  • Assessment of TRAF2 copy number gain and rearrangements.
  • Functional studies involving TRAF2 suppression and phosphorylation analysis.

Main Results:

  • TRAF2 was identified as an oncogene recurrently amplified and rearranged in 15% of human epithelial cancers.
  • Suppression of TRAF2 inhibited cancer cell proliferation, NF-κB activation, anchorage-independent growth, and tumorigenesis.
  • Cancer cell survival was dependent on both TRAF2 and NF-κB.
  • Phosphorylation of TRAF2 at serine 11 was essential for the survival of TRAF2-amplified cancer cells.

Conclusions:

  • TRAF2 is a frequently amplified oncogene in human epithelial cancers.
  • TRAF2 plays a critical role in cancer cell proliferation, survival, and tumorigenesis.
  • Targeting TRAF2 may represent a therapeutic strategy for cancers with TRAF2 amplification.

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