An Inflammatory Mediator, Prostaglandin E2, in Colorectal Cancer

被引:96
作者
Wang, Dingzhi [1 ]
DuBois, Raymond N. [1 ,2 ]
机构
[1] Arizona State Univ, Ctr Inflammat & Canc, Biodesign Inst, Tempe, AZ 85287 USA
[2] Arizona State Univ, Dept Biol & Chem, Tempe, AZ 85287 USA
基金
美国国家卫生研究院;
关键词
Colorectal cancer; risk factors; cyclooxygenase-derived prostaglandin E-2 (PGE(2)); tumor-induced immunosuppression; KILLER-CELL-ACTIVITY; REGULATORY T-CELLS; TUMOR-ASSOCIATED MACROPHAGES; ENDOTHELIAL GROWTH-FACTOR; MYELOID SUPPRESSOR-CELLS; DENDRITIC CELLS; MAST-CELLS; 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE; IN-VIVO; CYCLOOXYGENASE-2; INHIBITOR;
D O I
10.1097/PPO.0000000000000003
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
It is widely accepted that intake of dietary fats and chronic inflammation are risk factors for developing colorectal cancer. Arachidonic acid is a major component of animal fats, and the bioactive lipids produced from this substrate play critical roles in a variety of biologic processes, including cancer. Cyclooxygenase-derived prostaglandin E-2 is a known proinflammatory lipid mediator that promotes tumor progression. Metabolism of arachidonic acid by the cyclooxygenase pathway provides one mechanism for the contribution of dietary fats and chronic inflammation to carcinogenesis. In this review, we highlight recent advances in our understanding of how a proinflammatory mediator prostaglandin E-2 promotes colorectal cancer immune evasion. These findings may provide a rationale for the development of new therapeutic approaches to subvert tumor-induced immunosuppression.
引用
收藏
页码:502 / 510
页数:9
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