Effects of Extract of Angelica Sinensis (CB-1) on Hypoxia-Induced Hypoxia Inducible Factor 1 Expression in Human Bladder Cancer Cells and Angiogenesis in Chicken chorioallantoic membrane

碩士 === 國防醫學院 === 生理學研究所 === 96 === Cancer cell possess many special characteristics including rapid proliferation and resistant to apoptosis in a hypoxemic environment. Previous studies have shown that activation of hypoxia-inducible factor 1alpha (HIF-1) during hypoxia, triggering various genes ex...

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Bibliographic Details
Main Authors: Shu-Ni Hsieh, 謝淑妮
Other Authors: Tz-Chong Chou
Format: Others
Language:zh-TW
Published: 2008
Online Access:http://ndltd.ncl.edu.tw/handle/73166105510474742049
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Summary:碩士 === 國防醫學院 === 生理學研究所 === 96 === Cancer cell possess many special characteristics including rapid proliferation and resistant to apoptosis in a hypoxemic environment. Previous studies have shown that activation of hypoxia-inducible factor 1alpha (HIF-1) during hypoxia, triggering various genes expression including vascular endothelial growth factor (VEGF), plays an important role in tumor angiogenesis and progression. Recent studies have indicated that acetone extract of Angelica sinensis (CB-1) has an antiproliferative effect and induces apoptosis in human cancer cells. However, effect of CB-1 on HIF-1expression and angiogenesis in human bladder cancer cell is still unreported. Therefore, the aim of this study was to determine in hypoxia condition, whether CB-1 inhibits HIF-1expresson in human bladder cancer T24 cell and angiogenesis in the chicken chorioallantoic membrane (CAM) and further investigated the possible mechanisms involved. Our results showed that treatment with CB-1 dose-dependently inhibited hypoxia-induced HIF-1, VEGF expression and ROS formation. In addition, the hypoxia-induced cell migration was also reduced by CB-1. In CAM assay, CB-1 also inhibited hypoxia- and tumor-induced vascular formation as well. In conclusion, we demonstrate that CB-1 may be a potential anti-angiogenesis drug through inhibition of HIF-1expression and subsequent VEGF formation.