IR@PKUHSC  > 北京大学基础医学院  > 病理学系
学科主题基础医学
Basic FGF augments hypoxia induced HIF-1-alpha expression and VEGF release in T47D breast cancer cells
Shi, Yong-Hong; Bingle, Lynne; Gong, Li-Hua; Wang, Yu-Xiang; Corke, Kevin P.; Fang, Wei-Gang
关键词hypoxia inducible factor 1 alpha VEGF bFGF PI3K angiogenesis hypoxia
刊名PATHOLOGY
2007-08-01
DOI10.1080/00313020701444549
39期:4页:396-400
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pathology
研究领域[WOS]Pathology
关键词[WOS]ENDOTHELIAL GROWTH-FACTOR ; INDUCIBLE FACTOR (HIF)-1-ALPHA ; TUMOR ANGIOGENESIS ; HIF-1 ACTIVATION ; FIBROBLAST ; BFGF ; INDUCTION ; HIF-2-ALPHA ; INVOLVEMENT ; MODULATION
英文摘要

Aim: Both hypoxia inducible factor 1 (HIF-1) and basic fibroblast growth factor (bFGF) play important roles in tumour angiogenesis. This study was designed to clarify the cooperative effect of these two mediators in induction of vascular endothelial cell growth factor (VEGF) release from breast cancer and probe possible mechanisms involved.

Methods: Release of VEGF from a breast cancer cell line (T47D) was quantitated by enzyme linked immunosorbent assay (ELISA). Expression of HIF-1 and ERK was assayed using Western blotting. Transient transfection and dual luciferase reporter assay were used to study HIF-1 transactivity.

Results: The data showed that hypoxia induced the expression of HIF-1 alpha protein, the transactivity of HIF-1 and the release of VEGF. bFGF further augmented these hypoxic inductions. The PI3K pathway was required for these processes as demonstrated by application of PI3Kinase inhibitor (LY294002) or mutant construct transfections. In contrast, the MEK1 inhibitor PD98059 showed no effect on either activation of HIF-1 or VEGF release, which is in agreement with our finding that ERK1/2 was not activated by hypoxia. Under hypoxic conditions, bFGF activated the MEK1/ERK pathway. PD98059 blocked the activation of ERK1/2 and suppressed bFGF-induced HIF-1 transactivity, yet the protein expression of HIF-1 alpha or VEGF release was not affected by PD98059.

Conclusion: bFGF augments hypoxia induced VEGF release mainly through the PI3K pathway and partly depending on HIF-1 activity. Elucidation of this mechanism may provide a new target for anti-angiogenesis in cancer therapy.

语种英语
WOS记录号WOS:000248592800003
引用统计
被引频次:45[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61607
专题北京大学基础医学院_病理学系
作者单位1.Inner Mongolia Med Coll, Beijing, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Beijing, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Dept Pathol, Beijing 100083, Peoples R China
4.Univ Sheffield, Sch Med, Div Genom Med, Sheffield S1 3JD, S Yorkshire, England
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GB/T 7714
Shi, Yong-Hong,Bingle, Lynne,Gong, Li-Hua,et al. Basic FGF augments hypoxia induced HIF-1-alpha expression and VEGF release in T47D breast cancer cells[J]. PATHOLOGY,2007,39(4):396-400.
APA Shi, Yong-Hong,Bingle, Lynne,Gong, Li-Hua,Wang, Yu-Xiang,Corke, Kevin P.,&Fang, Wei-Gang.(2007).Basic FGF augments hypoxia induced HIF-1-alpha expression and VEGF release in T47D breast cancer cells.PATHOLOGY,39(4),396-400.
MLA Shi, Yong-Hong,et al."Basic FGF augments hypoxia induced HIF-1-alpha expression and VEGF release in T47D breast cancer cells".PATHOLOGY 39.4(2007):396-400.
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