Cdk5 Regulates Vascular Endothelial Growth Factor Expression through Androgen Receptor Activation in Prostate Cancer Cells

碩士 === 國立中興大學 === 生命科學系所 === 104 === Angiogenesis is an important function in tumor development. In hypoxia condition, angiogenesis begins because of Vascular endothelial growth factor (VEGF) is regulated by hypoxia-inducible factor-1α (HIF-1α). Androgen receptor (AR) plays an important role in the...

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Bibliographic Details
Main Authors: Chun-Chih Wang, 王俊智
Other Authors: Ho-Lin
Format: Others
Language:zh-TW
Published: 2015
Online Access:http://ndltd.ncl.edu.tw/handle/kdjnkb
Description
Summary:碩士 === 國立中興大學 === 生命科學系所 === 104 === Angiogenesis is an important function in tumor development. In hypoxia condition, angiogenesis begins because of Vascular endothelial growth factor (VEGF) is regulated by hypoxia-inducible factor-1α (HIF-1α). Androgen receptor (AR) plays an important role in the early stage of prostate cancer development. Our previous finding indicates that cyclin-dependent kinase 5 (Cdk5) is able to phosphorylate Ser81 site of AR in order to trigger AR activation and promote proliferation of prostate cancer cells. In addition, previous study suggested that androgen up-regulates VEGF expression through AR activation and it''s binding ability on androgen response element (ARE) of VEGF promoter. However, the mechanism between Cdk5 and VEGF regulation though AR activation in prostate cancer cells is poorly understood. In this study, Cdk5 overexpression could activate AR activation through Ser81-AR phosphorylation in order to up-regulate VEGF expression in prostate cancer cells. In conclusion, Cdk5 might enhance VEGF expression through AR activation in androgen-dependent prostate cancer cells. This finding indicates that Cdk5 might play an important role in regulating angiogenesis of prostate cancer.