CXCR2-dependent endothelial progenitor cell mobilization in pancreatic cancer growth

Aihua Li; Xiao J. Cheng; Aune Moro; Rakesh K. Singh; Oscar Joe Hines; Guido Eibl

doi:10.1593/tlo.10184

CXCR2-dependent endothelial progenitor cell mobilization in pancreatic cancer growth

Aihua Li, Xiao J. Cheng, Aune Moro, Rakesh K. Singh, Oscar Joe Hines, Guido Eibl

Research output: Contribution to journal › Article › peer-review

37 Scopus citations

Abstract

Neovascularization is essential for tumor growth. We have previously reported that the chemokine receptor CXCR2 is an important regulator in tumor angiogenesis. Here we report that the mobilization of bone marrow (BM)- derived endothelial progenitor cells (EPCs) is impaired in CXCR2 knockout mice harboring pancreatic cancers. The circulating levels of EPCs (positive for CD34, CD117, CD133, or CD146) are decreased in the bone marrow and/or blood of tumor-bearing CXCR2 knockout mice. CXCR2 gene knockout reduced BM-derived EPC proliferation, differentiation, and vasculogenesis in vitro. EPCs double positive for CD34 and CD133 increased tumor angiogenesis and pancreatic cancer growth in vivo. In addition, CD133⁺ and CD146⁺ EPCs in human pancreatic cancer are increased compared with normal pancreas tissue. These findings indicate a role of BM-derived EPC in pancreatic cancer growth and provide a cellular mechanism for CXCR2 mediated tumor neovascularization.

Original language	English (US)
Pages (from-to)	20-28
Number of pages	9
Journal	Translational Oncology
Volume	4
Issue number	1
DOIs	https://doi.org/10.1593/tlo.10184
State	Published - Feb 2011

ASJC Scopus subject areas

Oncology
Cancer Research

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title = "CXCR2-dependent endothelial progenitor cell mobilization in pancreatic cancer growth",

abstract = "Neovascularization is essential for tumor growth. We have previously reported that the chemokine receptor CXCR2 is an important regulator in tumor angiogenesis. Here we report that the mobilization of bone marrow (BM)- derived endothelial progenitor cells (EPCs) is impaired in CXCR2 knockout mice harboring pancreatic cancers. The circulating levels of EPCs (positive for CD34, CD117, CD133, or CD146) are decreased in the bone marrow and/or blood of tumor-bearing CXCR2 knockout mice. CXCR2 gene knockout reduced BM-derived EPC proliferation, differentiation, and vasculogenesis in vitro. EPCs double positive for CD34 and CD133 increased tumor angiogenesis and pancreatic cancer growth in vivo. In addition, CD133+ and CD146+ EPCs in human pancreatic cancer are increased compared with normal pancreas tissue. These findings indicate a role of BM-derived EPC in pancreatic cancer growth and provide a cellular mechanism for CXCR2 mediated tumor neovascularization.",

author = "Aihua Li and Cheng, {Xiao J.} and Aune Moro and Singh, {Rakesh K.} and Hines, {Oscar Joe} and Guido Eibl",

note = "Funding Information: Address all correspondence to: Aihua Li, MD, PhD, Department of Surgery, David Geffen School of Medicine, University of California at Los Angeles, 675 Charles Young Dr S, MRL 2535, Los Angeles, CA 90095. E-mail: [email protected] 1This work was supported by grants R21 CA124609 (O.J. Hines) and R01 CA122042 (G. Eibl) from the National Institutes of Health. Received 24 June 2010; Revised 9 October 2010; Accepted 13 October 2010 Copyright {\textcopyright} 2011 Neoplasia Press, Inc. Open access under CC BY-NC-ND license. 1944-7124/11 DOI 10.1593/tlo.10184",

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AU - Eibl, Guido

N1 - Funding Information: Address all correspondence to: Aihua Li, MD, PhD, Department of Surgery, David Geffen School of Medicine, University of California at Los Angeles, 675 Charles Young Dr S, MRL 2535, Los Angeles, CA 90095. E-mail: [email protected] 1This work was supported by grants R21 CA124609 (O.J. Hines) and R01 CA122042 (G. Eibl) from the National Institutes of Health. Received 24 June 2010; Revised 9 October 2010; Accepted 13 October 2010 Copyright © 2011 Neoplasia Press, Inc. Open access under CC BY-NC-ND license. 1944-7124/11 DOI 10.1593/tlo.10184

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N2 - Neovascularization is essential for tumor growth. We have previously reported that the chemokine receptor CXCR2 is an important regulator in tumor angiogenesis. Here we report that the mobilization of bone marrow (BM)- derived endothelial progenitor cells (EPCs) is impaired in CXCR2 knockout mice harboring pancreatic cancers. The circulating levels of EPCs (positive for CD34, CD117, CD133, or CD146) are decreased in the bone marrow and/or blood of tumor-bearing CXCR2 knockout mice. CXCR2 gene knockout reduced BM-derived EPC proliferation, differentiation, and vasculogenesis in vitro. EPCs double positive for CD34 and CD133 increased tumor angiogenesis and pancreatic cancer growth in vivo. In addition, CD133+ and CD146+ EPCs in human pancreatic cancer are increased compared with normal pancreas tissue. These findings indicate a role of BM-derived EPC in pancreatic cancer growth and provide a cellular mechanism for CXCR2 mediated tumor neovascularization.

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CXCR2-dependent endothelial progenitor cell mobilization in pancreatic cancer growth

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