TNF receptor associated factor 6 (TRAF6) plays a critical role in the regulation of innate immune responses and adaptive immune responses. Though recent studies indicate that TRAF6 is involved in cancer, its precise role in cancer including colon cancer has not been extensively investigated and remains largely unknown. The purpose of this work is to determine the expression of TRAF6 in colon cancer as well as the possible role of it in proliferation and apoptosis of colon cancer cells. Fifty colon cancer tissues paired with their adjacent non-cancerous tissues were analyzed. TRAF6 expression is upregulated in cancers (P=0.000), which is correlated with tumor grades (P=0.012). The tumor tissue-array analysis also indicates that expression of TRAF6 is upregulated in colon cancer (P=0.000), but the TRAF6 upregulation has no association with patients' survival rate (P=0.055). We found that knockdown of TRAF6 blocks proliferation of colon cancer cells through cyclin D1. Different from other reports, in our experiments knockdown of TRAF6 alone has little effect on survival of colon cancer cells examined. Knockdown of TRAF6 sensitizes the cells to treatment of the conventional anti-cancer drugs 5-fluorouracil and etoposide. Thus, inhibition of TRAF6 may improve the therapeutic treatment of these drugs. Together, our data suggest that TRAF6 promotes proliferation of colon cancer cells and it may serve as a potential target for therapy of colon cancer.
Keywords: Cell proliferation; Colon cancer; TRAF6; Tumorigenesis.
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