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In vitro study of HIF-1 activation and VEGF release by bFGF in the T47D breast cancer cell line under normoxic conditions: involvement of PI-3K/Akt and MEK1/ERK pathways
Shi, YH; Wang, YX; Bingle, L; Gong, LH; Heng, WJ; Li, Y; Fang, WG
关键词hypoxia-inducible factor 1 alpha angiogenesis VEGF bFGF breast tumour
刊名JOURNAL OF PATHOLOGY
2005-03-01
DOI10.1002/path.1734
205期:4页:530-536
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Pathology
研究领域[WOS]Oncology ; Pathology
关键词[WOS]ENDOTHELIAL GROWTH-FACTOR ; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA ; TUMOR ANGIOGENESIS ; FACTOR RECEPTOR ; FACTOR 1-ALPHA ; EXPRESSION ; FIBROBLAST ; INDUCTION ; MODULATION ; FACTOR-2
英文摘要

Hypoxia-inducible factor (HIF) is critical in the modulation of tumour angiogenesis in response to hypoxia. In the present study, the mechanisms underlying basic fibroblast growth factor (bFGF)-induced activation of HIF-1 and the subsequent release of vascular endothelial growth factor (VEGF) in a human breast cancer cell line (T47D) under normoxic conditions were explored. The data show that HIF-1 alpha expression is induced by bFGF in a dose- and time-dependent fashion, while increased HIF-1 alpha protein expression and transactivity of HIF-1 are due to the phosphorylation of Akt by bFGF, as indicated by application of the phosphatidylinositol 3-kinase (PI-3K) inhibitor LY294002. The data also show that the MEK1 (mitogen-activated protein kinase kinase-1)/ERK (extracellular signal-regulated kinase) pathway is only involved in bFGF-induced transactivity of HIF-1, but not HIF1 alpha expression, indicating roles for both the PI-3K/Akt and the MEK1/ERK pathways in bFGF activity. In addition, the translation inhibitor cycloheximide confirmed that bFGF-induced HIF-1 alpha protein expression was due to de novo protein synthesis. In contrast, p38 was not required for the expression of HIF-1 alpha or HIF-1 transactivity, although significant phosphorylation of p38 was observed after bFGF treatment. Treatment of the cells with bFGF increased the amount of VEGF release, and this could be suppressed by either PD98059 or LY294002, suggesting the presence of a HIF-1 alpha-dependent pathway for bFGF-induced VEGF production. In conclusion, the PI-3K/Akt and MEK1/ERK pathways, in a potentially independent and co-operative fashion, can modulate HIF-1 activation by bFGF. Further studies will pinpoint whether HIF-1 is the transcriptional factor responsible for the increased VEGF production following bFGF treatment of breast tumour cells. Copyright (C) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley H Sons, Ltd.

语种英语
WOS记录号WOS:000227505600015
引用统计
被引频次:61[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/400002259/59990
专题基础医学院_病理学系
作者单位1.Peking Univ, Hlth Sci Ctr, Dept Pathol, Beijing 100083, Peoples R China
2.Inner Mongolia Med Coll, Dept Pathol, Huhhot, Mongol Peo Rep
3.Univ Sheffield, Sch Med, Div Genom Med, Sheffield S10 2TN, S Yorkshire, England
推荐引用方式
GB/T 7714
Shi, YH,Wang, YX,Bingle, L,et al. In vitro study of HIF-1 activation and VEGF release by bFGF in the T47D breast cancer cell line under normoxic conditions: involvement of PI-3K/Akt and MEK1/ERK pathways[J]. JOURNAL OF PATHOLOGY,2005,205(4):530-536.
APA Shi, YH.,Wang, YX.,Bingle, L.,Gong, LH.,Heng, WJ.,...&Fang, WG.(2005).In vitro study of HIF-1 activation and VEGF release by bFGF in the T47D breast cancer cell line under normoxic conditions: involvement of PI-3K/Akt and MEK1/ERK pathways.JOURNAL OF PATHOLOGY,205(4),530-536.
MLA Shi, YH,et al."In vitro study of HIF-1 activation and VEGF release by bFGF in the T47D breast cancer cell line under normoxic conditions: involvement of PI-3K/Akt and MEK1/ERK pathways".JOURNAL OF PATHOLOGY 205.4(2005):530-536.
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