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TRAF2 is a crucial adaptor protein involved in various signaling pathways. However, its biological functions in nasopharyngeal carcinoma (NPC) remain largely unknown. In the present study, we found that TRAF2 was overexpressed in nasopharyngeal carcinoma (NPC) cells. Knockdown of TRAF2 with shRNA significantly suppressed NPC cell proliferation and colony formation. The growth of xenograft tumor significantly reduced after TRAF2 was silenced. Conversely, the ectopic overexpression of TRAF2 significantly promoted cell proliferation and anchorage-independent growth. In TRAF2 knockdown cells, EGF-induced activation of transcriptional factors, including MSK1, CREB, and ATF2, markedly decreased. Accordingly, the transcriptional activity of AP-1 was substantially decreased in TRAF2-deficient cells. With the suppression of gene transcription, the expression of cyclin D1 was significantly impaired, which gave rise to the G0/G1 cell cycle arrest. Moreover, the overexpression of TRAF2 in NPC cells was associated with resistance to irradiation, and the potency of irradiation was substantially enhanced after TRAF2 was knocked down. Briefly, our studies demonstrated that TRAF2 had a crucial role in NPC development, and it might be of great potential to targeting TRAF2 for NPC prevention and treatment.

TRAF2 Knockdown in Nasopharyngeal Carcinoma Induced Cell Cycle Arrest and Enhanced the Sensitivity to Radiotherapy