165) 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. |
PMID:24362534 DOI:10.1038/onc.2013.543 |
2015 Oncogene |
* TRAF2 is an NF-κB-activating oncogene in epithelial cancers. |
- 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. |
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(2)48 cells | (15)6 tissues | (28)3 patients, | (41)2 growth |
(3)33 and | (16)5 cells, | (29)3 research | (42)2 initiation |
(4)32 cell | (17)5 progression | (30)3 was | (43)2 prevention |
(5)23 patients | (18)5 registries | (31)2 (GC) | (44)2 registry |
(6)15 in | (19)4 at | (32)2 biology | (45)2 study |
(7)14 is | (20)4 deaths | (33)2 but | (46)2 susceptibility |
(8)12 risk | (21)4 has | (34)2 can | (47)2 than |
(9)12 screening | (22)4 mortality | (35)2 care | (48)2 treated |
(10)12 stem | (23)3 (CRC) | (36)2 development | (49)2 treatment |
(11)9 survivors | (24)3 as | (37)2 diagnostic | (50)2 using |
(12)7 with | (25)3 cases | (38)2 drug | |
(13)6 are | (26)3 metabolism | (39)2 drugs |
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