cxcl7-mediated stimulation of lymphangiogenic factors vegf-c, vegf-d in human breast cancer cellsvegf-c cxcl7-mediated lymphangiogenic的刺激因素,vegf-d在人类乳腺癌细胞.pdfVIP

cxcl7-mediated stimulation of lymphangiogenic factors vegf-c, vegf-d in human breast cancer cellsvegf-c cxcl7-mediated lymphangiogenic的刺激因素,vegf-d在人类乳腺癌细胞.pdf

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cxcl7-mediated stimulation of lymphangiogenic factors vegf-c, vegf-d in human breast cancer cellsvegf-c cxcl7-mediated lymphangiogenic的刺激因素,vegf-d在人类乳腺癌细胞

Hindawi Publishing Corporation Journal of Oncology Volume 2010, Article ID 939407, 10 pages doi:10.1155/2010/939407 Research Article CXCL7-Mediated Stimulation of Lymphangiogenic Factors VEGF-C, VEGF-D in Human Breast Cancer Cells Minghuan Yu,1 Richard Berk,2 and Mary Ann Kosir1, 3, 4 1 Department of Surgery, Wayne State University, Detroit, MI 48201, USA 2 Department of Immunology and Microbiology, Wayne State University, Detroit, MI 48201, USA 3 Surgical Service, John D. Dingell VA Medical Center, Detroit, MI 48201, USA 4 Breast Biology Program, Karmanos Cancer Institute, Detroit, MI 48201, USA Correspondence should be addressed to Mary Ann Kosir, kosirm@ Received 1 November 2009; Revised 27 March 2010; Accepted 3 May 2010 Academic Editor: Arkadiusz Dudek Copyright © 2010 Minghuan Yu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Increased expression of lymphangiogenesis factors VEGF-C/D and heparanase has been correlated with the invasion of cancer. Furthermore, chemokines may modify matrix to facilitate metastasis, and they are associated with VEGF-C and heparanase. The chemokine CXCL7 binds heparin and the G-protein-linked receptor CXCR2. We investigatedthe effect of CXCR2 blockade on the expression of VEGF-C/D, heparanase, and on invasion. CXCL7 siRNA and a specific antagonist of CXCR2 (SB225002) were used to treat CXCL7 stably transfected MCF10AT cells. Matrigel invasion assays were performed. VEGF-C/D expression and secretion were determined by real-time PCR and ELISA assay, and heparanase activity was quantified by ELISA. SB225002 blocked VEGF- C/D expression and secretion (P .01

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