Inflammation as a tumor promoter in cancer induction
Inflammation as a tumor promoter in cancer induction
复制标题
DOI：
10.1016/j.semcancer.2004.06.006
复制
发表时间：
2004-12-01
影响因子：
14.5
通讯作者：
Schreiber, H
中科院分区：
文献类型：
--
作者：
Philip, M;Rowley, DA;Schreiber, H
已经描述了炎症对癌症的相反作用。急性炎症通常抵消癌症发展，而慢性炎症促进癌症发展。正如p53通路的失活在瘤形成中可能是普遍的，相反，NF κ B通路的激活可能在癌发生中是频繁的，并且是炎症和促进的需要。TNF是一种关键的促炎细胞因子，当与TNF受体1（TNFR 1）结合时，可能导致存活或凋亡，这取决于决定所形成复合物类型的生化修饰;一种复合物导致NF κ B活化并提供细胞存活信号（促癌），而另一种（修饰的）复合物招募半胱天冬酶并导致凋亡（抗癌）。Fas-配体（FasL）-Fas相互作用也可由于类似的机制而导致对致癌作用的相反作用。虽然IL-6抵消细胞凋亡并可促进癌症发展，但干扰素可增加DNA修复并稳定p53，从而具有抗癌作用。(C)2004爱思唯尔有限公司保留所有权利。
Opposing effects of inflammation on cancer have been described. Acute inflammation usually counteracts cancer development, while chronic inflammation promotes cancer development. Just as inactivation of the p53 pathway may be universal in the neoplasia, the activation of the NFkappaB pathway may, conversely, be frequent in carcinogenesis, and a requirement for inflammation and promotion. TNF, a key pro-inflammatory cytokine when binding to TNF receptor 1 (TNFR 1), may cause survival or apoptosis, dependent on biochemical modifications that determine the type of complex formed; one complex causes NFkappaB activation and gives a cell survival signal (pro-oncogenic), while the other (modified) complex recruits caspases and causes apoptosis (anti-oncogenic). Fas-ligand (FasL)-Fas interaction can also result in opposing effects on carcinogenesis due to similar mechanisms. While IL-6 counteracts apoptosis and can promote cancer development, interferons can increase DNA repair and stabilize p53, thereby be anti-oncogenic. (C) 2004 Elsevier Ltd. All rights reserved.