Int. J. Mol. Sci. 2013, 14(7), 13329-13345; doi:10.3390/ijms140713329
Article

Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers

1 Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan 2 Department of Urology, Buddhist Tzu Chi General Hospital Taichung Branch, Taichung 42743, Taiwan 3 School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan 4 Department of Pharmacology, School of Medicine, China Medical University, Taichung 40402, Taiwan 5 Department of Biotechnology, College of Health Science, Asia University, Taichung 41354, Taiwan
* Author to whom correspondence should be addressed.
Received: 10 May 2013; in revised form: 4 June 2013 / Accepted: 5 June 2013 / Published: 26 June 2013
(This article belongs to the Section Biochemistry, Molecular Biology and Biophysics)
PDF Full-text Download PDF Full-Text [1509 KB, uploaded 26 June 2013 11:18 CEST]
Abstract: Prostate cancer is the most commonly diagnosed malignancy in men and shows a predilection for metastasis to distant organs. Bradykinin (BK) is an inflammatory mediator and has recently been shown to mediate tumor growth and metastasis. The adhesion molecule intercellular adhesion molecule-1 (ICAM-1) plays a critical role during tumor metastasis. The aim of this study was to examine whether BK promotes prostate cancer cell migration via ICAM-1 expression. The motility of cancer cells was increased following BK treatment. Stimulation of prostate cancer cells with BK induced mRNA and protein expression of ICAM-1. Transfection of cells with ICAM-1 small interfering RNA reduced BK-increased cell migration. Pretreatment of prostate cancer cells with B2 receptor, phosphatidylinositol 3-kinase (PI3K), Akt, and activator protein 1 (AP-1) inhibitors or mutants abolished BK-promoted migration and ICAM-1 expression. In addition, treatment with a B2 receptor, PI3K, or Akt inhibitor also reduced BK-mediated AP-1 activation. Our results indicate that BK enhances the migration of prostate cancer cells by increasing ICAM-1 expression through a signal transduction pathway that involves the B2 receptor, PI3K, Akt, and AP-1. Thus, BK represents a promising new target for treating prostate cancer metastasis.
Keywords: bradykinin; migration; ICAM-1; prostate cancer

Article Statistics

Load and display the download statistics.

Citations to this Article

Cite This Article

MDPI and ACS Style

Yu, H.-S.; Lin, T.-H.; Tang, C.-H. Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers. Int. J. Mol. Sci. 2013, 14, 13329-13345.

AMA Style

Yu H-S, Lin T-H, Tang C-H. Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers. International Journal of Molecular Sciences. 2013; 14(7):13329-13345.

Chicago/Turabian Style

Yu, Hsin-Shan; Lin, Tien-Huang; Tang, Chih-Hsin. 2013. "Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers." Int. J. Mol. Sci. 14, no. 7: 13329-13345.

Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert