Bradykinin promotes vascular endothelial growth factor expression and increases angiogenesis in human prostate cancer cells

ASIA unversity > 管理學院 > 國際企業學系 > 期刊論文 > Item 310904400/79684

Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79684

Title:	Bradykinin promotes vascular endothelial growth factor expression and increases angiogenesis in human prostate cancer cells
Authors:	Hsin-Shan Yu(Hsin-Shan Yu)、Shih-Wei Wan(Shih-Wei Wang)、An-Chen Chan(An-Chen Chang)、Huai-Ching T(Huai-Ching Tai)、Hung-I Yeh(Hung-I Yeh)、Yu-Min Lin(Yu-Min Lin)、湯智昕(Chih-Hsin, Tang)*
Contributors:	生物科技學系
Keywords:	Angiogenesis;Bradykinin;Prostate cancer;VEGF
Date:	2014-01
Issue Date:	2014-06-05 03:52:59 (UTC+0)
Abstract:	Prostate cancer is the most commonly diagnosed malignancy in men and shows a tendency for metastasis to distant organs. Angiogenesis is required for metastasis. Bradykinin (BK) is an inflammatory mediator involved in tumor growth and metastasis, but its role in vascular endothelial growth factor (VEGF) expression and angiogenesis in human prostate cancer remains unknown. The aim of this study was to examine whether BK promotes prostate cancer angiogenesis via VEGF expression. We found that exogenous BK increased VEGF expression in prostate cancer cells and further promoted tube formation in endothelial progenitor cells and human umbilical vein endothelial cells. Pretreatment of prostate cancer with B2 receptor antagonist or small interfering RNA (siRNA) reduced BK-mediated VEGF production. The Akt and mammalian target of rapamycin (mTOR) pathways were activated after BK treatment, and BK-induced VEGF expression was abolished by the specific inhibitor and siRNA of the Akt and mTOR cascades. BK also promoted nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) activity. Importantly, BK knockdown reduced VEGF expression and abolished prostate cancer cell conditional medium-mediated angiogenesis. Taken together, these results indicate that BK operates through the B2 receptor, Akt, and mTOR, which in turn activate NF-κB and AP-1, activating VEGF expression and contributing to angiogenesis in human prostate cancer cells. Copyright © 2013 Elsevier Inc. All rights reserved.
Relation:	BIOCHEMICAL PHARMACOLOGY
Appears in Collections:	[國際企業學系] 期刊論文

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