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Bradykinin enhances cell migration in human chondrosarcoma cells through BK receptor signaling pathways

✍ Scribed by Wei-Hung Yang; Jung-Tzu Chang; Sheng-Feng Hsu; Te-Mao Li; Der-Yang Cho; Chun-Yin Huang; Yi-Chin Fong; Chih-Hsin Tang

Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
396 KB
Volume
109
Category
Article
ISSN
0730-2312

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✦ Synopsis

Abstract

Bradykinin (BK) is an inflammatory mediator, and shows elevated levels in regions of severe injury 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 α2β1 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 B2 BK receptor siRNA or antagonist. Activations of phospholipase C (PLC), protein kinase Cδ (PKCδ), and NF‐κB pathways after BK treatment was demonstrated, and BK‐induced integrin expression and migration activity was inhibited by the specific inhibitor of PLC, PKCδ, and NF‐κB cascades. Taken together, our results indicated that BK enhances the migration of chondrosarcoma cells by increasing α2β1 integrin expression through the BK receptors/PLC/PKCδ/NF‐κB signal transduction pathway. J. Cell. Biochem. 109: 82–92, 2010. © 2009 Wiley‐Liss, Inc.

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