EMMPRIN regulates tumor growth and metastasis by recruiting bone marrow-derived cells through paracrine signaling of SDF-1 and VEGF
Metrics: PDF 1444 views | HTML 1446 views | ?
Yanke Chen1,2, Xingchun Gou2,3, Derek Kai Kong2, Xiaofei Wang1, Jianhui Wang4, Zeming Chen2, Chen Huang1, Jiangbing Zhou2,5
1Experiment Center of Biomedical Research School of Medicine, Xi’an Jiaotong University, Xi’an 710061, P. R. China
2Department of Neurosurgery, Yale University, New Haven, CT 06511, USA
3Laboratory of Cell Biology and Translational Medicine, Xi’an Medical University, Xi’an 710021, P. R. China
4Department of Pathology, Yale University, New Haven, CT 06511, USA
5Department of Biomedical Engineering, Yale University, New Haven, CT 06510, USA
Jiangbing Zhou, e-mail: firstname.lastname@example.org
Chen Huang, e-mail: email@example.com
Keywords: EMMPRIN, bone marrow-derived cells, SDF-1, VEGF, tumor growth and metastasis
Received: May 06, 2015 Accepted: September 11, 2015 Published: September 22, 2015
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.