EMMPRIN regulates tumor growth and metastasis by recruiting bone marrow-derived cells through paracrine signaling of SDF-1 and VEGF

被引：31

作者：

Chen, Yanke ^{[1
,2
]}

Gou, Xingchun ^{[2
,3
]}

Kong, Derek Kai ^{[2
]}

Wang, Xiaofei ^{[1
]}

Wang, Jianhui ^{[4
]}

Chen, Zeming ^{[2
]}

Huang, Chen ^{[1
]}

Zhou, Jiangbing ^{[2
,5
]}

机构：

[1] Xi An Jiao Tong Univ, Sch Med, Expt Ctr Biomed Res, Xian 710061, Peoples R China

[2] Yale Univ, Dept Neurosurg, New Haven, CT 06511 USA

[3] Xian Med Univ, Lab Cell Biol & Translat Med, Xian 710021, Peoples R China

[4] Yale Univ, Dept Pathol, New Haven, CT 06511 USA

[5] Yale Univ, Dept Biomed Engn, New Haven, CT 06510 USA

来源：

ONCOTARGET | 2015年 / 6卷 / 32期

基金：

中国国家自然科学基金;

关键词：

EMMPRIN; bone marrow-derived cells; SDF-1; VEGF; tumor growth and metastasis; ENDOTHELIAL-CELLS; CHEMOKINE RECEPTOR-4; CANCER; EXPRESSION; CD147; ANGIOGENESIS; OVEREXPRESSION; VASCULOGENESIS; PROGENITORS; CXCR4;

D O I：

10.18632/oncotarget.5331

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

EMMPRIN, a cell adhesion molecule highly expressed in a variety of tumors, is associated with poor prognosis in cancer patients. Mechanistically, EMMPRIN has been characterized to contribute to tumor development and progression by controlling the expression of MMPs and VEGF. In the present study, by using fluorescently labeled bone marrow-derived cells (BMDCs), we found that the down-regulation of EMMPRIN expression in cancer cells reduces tumor growth and metastasis, and is associated with the reduced recruitment of BMDCs. Further protein profiling studies suggest that EMMPRIN controls BMDC recruitment through regulating the secretion of soluble factors, notably, VEGF and SDF-1. We demonstrate that the expression and secretion of SDF-1 in tumor cells are regulated by EMMPRIN. This study reveals a novel mechanism by which EMMPRIN promotes tumor growth and metastasis by recruitment of BMDCs through controlling secretion and paracrine signaling of SDF-1 and VEGF.

引用

页码：32575 / 32585

页数：11

共 40 条

[1]

Stromal cell-derived factor-1α plays a critical role in stem cell recruitment to the heart after myocardial infarction but is not sufficient to induce homing in the absence of injury [J].