English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90453/105672 (86%)
Visitors : 13104415      Online Users : 572
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79555

    Title: Bradykinin promotes vascular endothelial growth factor expression and increases angiogenesis in human prostate cancer cells
    Authors: Yu, Hsin-Shan;Yu, Hsin-Shan;Wan, Shih-Wei;Wang, Shih-Wei;Chan, An-Chen;Chang, An-Chen;Huai-Ching, T;Tai, Huai-Ching;Yeh, Hung-I;Yeh, Hung-I;Lin, Yu-Min;Lin, Yu-Min;湯智昕;Chih-Hsin, Tang
    Contributors: 生物科技學系
    Keywords: Angiogenesis;Bradykinin;Prostate cancer;VEGF
    Date: 2014-01
    Issue Date: 2014-06-04 10:16:15 (UTC+8)
    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.
    Relation: BIOCHEMICAL PHARMACOLOGY, V.87(2)243–253
    Appears in Collections:[生物科技學系] 期刊論文

    Files in This Item:

    File SizeFormat

    All items in ASIAIR are protected by copyright, with all rights reserved.

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback