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学科主题: 基础医学
题名:
Basic FGF augments hypoxia induced HIF-1-alpha expression and VEGF release in T47D breast cancer cells
作者: 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
发表日期: 2007-08-01
DOI: 10.1080/00313020701444549
卷: 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
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61607
Appears in Collections:基础医学院_病理学系_期刊论文

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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

Recommended Citation:
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.
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