Prostaglandin E2 regulates cellular migration via induction of vascular endothelial growth factor receptor-1 in HCA-7 human colon cancer cells

被引：39

作者：

Fujino, Hiromichi ^{[1
]}

Toyomura, Kaori ^{[1
]}

Chen, Xiao-bo ^{[2
]}

Regan, John W. ^{[2
]}

Murayama, Toshihiko ^{[1
]}

机构：

[1] Chiba Univ, Chem Pharmacol Lab, Grad Sch Pharmaceut Sci, Chuo Ku, Chiba 2608675, Japan

[2] Univ Arizona, Coll Pharm, Dept Pharmacol & Toxicol, Tucson, AZ 85721 USA

来源：

BIOCHEMICAL PHARMACOLOGY | 2011年 / 81卷 / 03期

关键词：

PGE(2); Human EP3 receptor; VEGFR-1; Colon cancer; Metastasis; TUMOR-GROWTH; EP2; ANGIOGENESIS; ACTIVATION; SUBTYPE; VEGF; TRANSDUCTION; EXPRESSION; PATHWAYS;

D O I：

10.1016/j.bcp.2010.11.001

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

An important event in the development of tumors is angiogenesis, or the formation of new blood vessels. Angiogenesis is also known to be involved in tumor cell metastasis and is dependent upon the activity of the vascular endothelial growth factor (VEGF) signaling pathway. Studies of mice in which the EP3 prostanoid receptors have been genetically deleted have shown a role for these receptors in cancer growth and angiogenesis. In the present study, human colon cancer HCA-7 cells were used as a model system to understand the potential role of EP3 receptors in tumor cell migration. We now show that stimulation of HCA-7 cells with PGE(2) enhanced the up-regulation of VEGF receptor-1 (VEGFR-1) expression by a mechanism involving EP3 receptor-mediated activation of phosphatidylinositol 3-kinase and the extracellular signal-regulated kinases. Moreover, the PGE2 stimulated increase in VEGFR-1 expression was accompanied by an increase in the cellular migration of HCA-7 cells. Given the known involvement of VEGFR-1 in cellular migration, our results suggest that EP3 receptors may contribute to tumor cell metastasis by increasing cellular migration through the up-regulation of VEGFR-1 signaling. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：379 / 387

页数：9

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