Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/69803
標題: Bradykinin Enhances Cell Migration in Human Chondrosarcoma Cells Through BK Receptor Signaling Pathways
作者: Yang, W.H.
Chang, J.T.
Hsu, S.F.
Li, T.M.
Cho, D.Y.
Huang, C.Y.
Fong, Y.C.
Tang, C.H.
關鍵字: bradykinin;chondrosarcoma;bk receptor;integrin;nf-kappa-b;integrin up-regulation;lung-cancer;alpha-v-beta-3;integrin;prostaglandin e-2;dependent pathway;local recurrence;prognostic value;breast-cancer;expression
Project: Journal of Cellular Biochemistry
期刊/報告no:: Journal of Cellular Biochemistry, Volume 109, Issue 1, Page(s) 82-92.
摘要: 
Bradykinin (BK) is an inflammatory mediator, and shows elevated levels in regions of severe in. jury and inflammatory diseases. BK has recently been shown to be involved in carcinogenesis and cancer progression. In this study, we found that BK increased the migration and the expression of alpha 2 beta 1 integrin in human chondrosarcoma cells. We also found that human chondrosarcoma tissues had significantly higher expression of the B1 and B2 receptors comparing to normal cartilage. BK-mediated migration and integrin up-regulation was attenuated by B1 and 132 BK receptor siRNA or antagonist. Activations of phospholipase C (PLC), protein kinase C delta (PKC delta), and NF-kappa B pathways after BK treatment was demonstrated, and BK-induced integrin expression and migration activity was inhibited by the specific inhibitor of PLC, PKC delta, and NF-kappa B cascades. Taken together, our results indicated that BK enhances the migration of chondrosarcoma cells by increasing alpha 2 beta 1 integrin expression through the BK receptors/PLC/PKC delta/NF-kappa B signal transduction pathway. J. Cell. Biochem. 109: 82-92, 2010. (C) 2009 Wiley-Liss, Inc.
URI: http://hdl.handle.net/11455/69803
ISSN: 0730-2312
DOI: 10.1002/jcb.22383
Appears in Collections:期刊論文

Show full item record
 

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.