Inflammasomes and intestinal tumorigenesis

Md. Hasan Zaki , Mohamed Lamkanfi , Thirumala-Devi Kanneganti
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引用次数: 16

Abstract

Colorectal cancer is a major health problem in developed countries. Chronic intestinal inflammation predisposes individuals to the development of colorectal cancer. The intracellular NOD-like receptors (NLRs) have emerged as crucial regulators of intestinal inflammation and colorectal tumorigenesis. Activation of several NLRs leads to the formation of a protein complex called the inflammasome, which then triggers the activation of the cysteine protease caspase-1 and the downstream maturation and secretion of the inflammatory cytokines interleukin (IL)-1β and -18. Defective inflammasome signaling in the gut contributes to colitis and colorectal tumorigenesis by increasing the permeability of the epithelial barrier, dysregulating the proliferation of epithelial cells, and inducing oncogenic mediators. In this review, we discuss our current knowledge on how the inflammasome protects against colorectal tumorigenesis.

炎性小体与肠道肿瘤发生
结直肠癌是发达国家的一个主要健康问题。慢性肠道炎症使个体易患结直肠癌。细胞内nod样受体(NLRs)已成为肠道炎症和结直肠肿瘤发生的重要调节因子。几个nlr的激活导致一种称为炎性体的蛋白质复合物的形成,然后触发半胱氨酸蛋白酶caspase-1的激活以及下游炎症细胞因子白细胞介素(IL)-1β和-18的成熟和分泌。肠道炎症小体信号的缺陷通过增加上皮屏障的通透性、调节上皮细胞的增殖和诱导致癌介质,有助于结肠炎和结直肠肿瘤的发生。在这篇综述中,我们讨论了目前关于炎性体如何防止结直肠肿瘤发生的知识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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