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Induction of vascular endothelial growth factor by peptidyl-prolyl isomerase Pin1 in breast cancer cells

Authors
Kim, Mi RaChoi, Hong SeokHeo, Tae-HweHwang, Sun WookKang, Keon Wook
Issue Date
2-May-2008
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
AP-1; HIF-1 alpha; Pin1; VEGF
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.369, no.2, pp.547 - 553
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
369
Number
2
Start Page
547
End Page
553
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/123554
DOI
10.1016/j.bbrc.2008.02.045
ISSN
0006-291X
Abstract
Pin1, a peptidyl-prolyl isomerase, is overexpressed in most types of cancer tissues and plays an important role in oncogenesis. We found that Pin1 increases the transcriptional activity and protein level of vascular endothelial growth factor (VEGF) in the human breast cancer cell line, MCF-7. Reporter gene analyses showed that Pin1 overexpression increased the reporter activities in cells transfected with reporters containing the VEGF gene promoter or with minimal reporters of activator protein-1 (AP-1) and hypoxia response element (HRE). VEGF reporter gene activity was significantly inhibited by either hypoxia-inducible factor-alpha (HIF-1 alpha) siRNA or AP-1 decoy ODN. Moreover, the reporter activities of the VEGF promoter, AP-1 and HRE in Pin1-/- mouse embryonic fibroblast (MEF) cells were decreased compared with those in wild-type Pin1 MEF cells. These results imply that Pin1 stimulates VEGF expression by activating HIF-1 alpha and AP-1, and suggest that Pin1 is a potential therapeutic target of angiogenesis during cancer development. (C) 2008 Published by Elsevier Inc.
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