Spliceosome protein Eftud2 promotes colitis-associated tumorigenesis by modulating inflammatory response of macrophage

• DOI: 10.1038/s41385-019-0184-y
• Publication Date: 2019-07-05T16:02:54Z
• Authors: Zhonglin Lv; Zhihong Wang; Longlong Luo; Yu Chen; Gencheng Han; Renxi Wang; He Xiao; Xinying Li; Chunmei Hou; Jiannan Feng; Beifen Shen; Yi Wang; Hui Peng; Renfeng Guo; Yan Li; Guojiang Chen
• Keywords: Pathogenesis

Alternative splicing (AS) of mRNA is known to be involved in regulation immune cell differentiation and activation. Elongation factor Tu GTP binding domain containing 2 (Eftud2) an AS potentially modulate innate response macrophages. In this study, we investigate its involvement the pathogenesis colitis-associated cancer (CAC). Using established mouse model CAC, show that Eftud2 constantly overexpressed colonic tissues as well infiltrating Myeloid-specific knockout remarkably suppresses chronic intestinal inflammation tumorigenesis, which associated with decreased production inflammatory cytokines tumorigenic factors. Repression colorectal tumor development Eftud2-deficient mice due impaired activation NF-κB signaling LPS-challenged Furthermore, alteration Eftud2-mediated involving components TLR4-NF-κB cascades underlies impairment Overall, these findings provide new insights into tight link between modulation signals may a therapeutic avenue for CAC treatment.