Prostaglandin E2 Signaling: Alternative Target for Glioblastoma?

被引：62
|
作者：
Jiang, Jianxiong [1 ]
Qiu, Jiange [1 ,2 ,3 ]
Li, Qianqian [1 ]
Shi, Zhi [2 ,3 ]
机构：
[1] Univ Cincinnati, Acad Hlth Ctr, James L Winkle Coll Pharm, Div Pharmaceut Sci, Cincinnati, OH 45267 USA
[2] Jinan Univ, Coll Life Sci & Technol, Natl Engn Res Ctr Genet Med, Guangdong Prov Key Lab Bioengn Med,Dept Cell Biol, Guangzhou 510632, Guangdong, Peoples R China
[3] Jinan Univ, Coll Life Sci & Technol, Guangdong Prov Key Lab Bioengn Med, Natl Engn Res Ctr Genet Med,Inst Biomed, Guangzhou 510632, Guangdong, Peoples R China
来源：
TRENDS IN CANCER | 2017年 / 3卷 / 02期
基金：
美国国家卫生研究院; 中国国家自然科学基金;
关键词：
GLIOMA-CELL GROWTH; RECEPTOR EP2; E SYNTHASE-1; INFLAMMATION; MICROGLIA; SURVIVAL; CANCER;
D O I：
10.1016/j.trecan.2016.12.002
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Elevated cyclooxygenase-2 (COX-2) and the associated inflammation within the brain contribute to glioblastoma development. However, medical use of COX inhibitors in glioblastoma treatment has been limited due to their well-documented vascular toxicity and inconsistent outcomes from recent human studies. Prostaglandin E2 (PGE2) has emerged as a principal mediator for COX-2 cascade-driven gliomagenesis. Are PGE(2) terminal synthases and receptors feasible therapeutic targets for glioblastoma?
引用
收藏
页码：75 / 78
页数：4
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