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Carcinogenesis Advance Access published online on February 28, 2008
Carcinogenesis, doi:10.1093/carcin/bgn045
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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Bone-derived SDF-1 stimulates IL-6 Release via CXCR4, ERK and NF-{kappa}B pathways and promoting osteoclastogenesis in human oral cancer cells

Chih-Hsin Tang1,*, Jing-Yuan Chuang3, Yi-Chin Fong5,7,8, Ming-Chei Maa6, Tzong-Der Way4 and Chien-Hui Hung2

1 Departments of Pharmacology, China Medical University, Taichung, Taiwan
2 Department of Microbiology, China Medical University, Taichung, Taiwan
3 Departments of Medical Laboratory Science and Biotechnology
4 Biological Science and Technology
7 School of Chinese Medicine
8 Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan
5 Department of Orthopaedics China Medical University Hospital, Taichung, Taiwan
6 Institute of Medical Science, China Medical University, Taichung, Taiwan

* Address correspondence to: Tang Chih-Hsin, Department of Pharmacology, College of Medicine, China Medical University, No. 91, Hsueh-Shih Road, Taichung, Taiwan, Tel: 886-4-22053366-2228, Fax: 886-4-22053764, E-mail: chtang{at}mail.cmu.edu.tw

Oral squamous cell carcinoma (SCC) has a striking tendency to invade to bone. The chemokine stromal cell-derived factor-1 (SDF-1) is constitutively secreted by osteoblasts and plays a key role in homing of hematopoietic cells to the bone marrow. IL-6 plays an important role in osteoclatogenesis. Herein, we found that SDF-1{alpha} increased the secretion of IL-6 in cultured human SCC cells, as shown by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay. SDF-1{alpha} also increased the surface expression of CXCR4 receptor in SCC cells. CXCR4-neutralizing antibody, CXCR4 specific inhibitor (AMD3100) or small interfering RNA against CXCR4 inhibited SDF-1{alpha}-induced increase IL-6 production. The transcriptional regulation of IL-6 by SDF-1{alpha} was mediated by phosphorylation of exracelluar signal-regulated kinases (ERK) and activation of the NF-{kappa}B components p65 and p50. The binding of p65 and p50 to the NF-{kappa}B element on the IL-6 promoter was enhanced by SDF-1{alpha}. In addition, IL-6 antibody antagonized the SCC-conditioned medium-increased osteoclastogenesis. These results suggested that SDF-1{alpha} from osteoblasts could induce release of IL-6 in human SCC cells via activation of CXCR4, ERK and NF-{kappa}B pathway and thereby promote osteoclastogenesis

Key Words: IL-6 • Oral cancer • Osteoblasts • SDF • NF-{kappa}B

Received November 9, 2007; revised January 21, 2008; accepted February 2, 2008.


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