偶氮甲烷
肥大细胞
炎症
癌症研究
癌变
炎症性肠病
结肠炎
免疫学
肿瘤微环境
生物
结直肠癌
发病机制
癌症
免疫系统
医学
病理
疾病
遗传学
作者
Ji‐Hyun Lee,Yong‐Deok Jeon,Mingjie Xin,Ji-Ye Lim,Young‐Mi Lee,Dae-Ki Kim
标识
DOI:10.1016/j.bbrep.2022.101253
摘要
Mast cells infiltrate the inflammatory microenvironment and regulate the production of many pro-inflammatory cytokines and mediators of inflammatory cell production to promote tumor development and growth in intestinal lesions. Currently, there are insufficient studies of the mediators and signaling pathways regulated by mast cells that influence the pathogenesis of colon cancer in inflamed colon tissue. This study aimed to confirm the role of mast cells in the incidence and growth of colitis-associated colon cancer (CAC) and to identify inflammation-mediated factors and signaling pathways related to tumor development. CAC was induced by the administration of azoxymethane (AOM) and dextran sodium sulfate (DSS) in mast cell-deficient (WBB6F1/J-W/WV) and mast cell–sufficient control (WBB6F1_+/+) mice. The results confirmed that mast cell-deficient mice exhibited less tumor formation than normal mice under the same conditions, and down-regulated expression of pro-inflammatory cytokines and mediators. Mast cells play an important role in tumor formation by regulating pro-inflammatory cytokines and inflammatory mediators in CAC, indicating that they can act as new targets for the prevention and treatment of CAC.
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