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学科主题: 临床医学
题名:
VEGF(165)b, an inhibitory splice variant of vascular endothelial growth factor, is down-regulated in renal cell carcinoma
作者: Bates, DO; Cui, TG; Doughty, JM; Winkler, M; Sugiono, M; Shields, JD; Peat, D; Gillatt, D; Harper, SJ
刊名: CANCER RESEARCH
发表日期: 2002-07-15
卷: 62, 期:14, 页:4123-4131
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology
研究领域[WOS]: Oncology
关键词[WOS]: QUANTITATIVE RT-PCR ; MESSENGER-RNA ; FACTOR ISOFORM ; EXPRESSION ; PERMEABILITY ; RECEPTOR ; KIDNEY ; TUMOR ; IDENTIFICATION ; ANGIOGENESIS
英文摘要:

Angiogenesis is essential for tumor growth. Vascular endothelial growth factor (VEGF) is the most potent growth factor of tumor neovas-culature, has been shown to be up-regulated in every tumor studied thus far, and is correlated with tumor stage and progression. To determine whether specific VEGF splice variants were differentially expressed in renal cell carcinomas, 18 polar tumor samples were analyzed by reverse transcription-PCR using primers designed to differentiate between VEGF splice variants. Control tissue was derived from the opposite normal pole. An amplicon of length consistent with the previously described variant VEGF(148) was found in normal kidney tissue. Subsequent sequencing revealed a new VEGF isoform formed by differential splicing from the end of exon 7 into the 3′ untranslated region of the mRNA. Cloning of this transcript showed that translation would result in a 165-amino acid peptide with an alternative terminal 6 amino acids, followed by a stop codon. We have termed this new isoform VEGF(165)b. This isoform was present in 17 of 18 normal kidney samples but only 4 of 18 cases from matched malignant tissue. VEGF(165)b was therefore expressed in a significantly higher proportion of normal tissue than malignant tissue from the same patients (P < 0.001). To determine the functional significance of this new isoform, we expressed the full-length protein in a heterologous expression system. Conditioned medium containing this isoform significantly and dose dependently inhibited VEGF (165)-mediated proliferation, migration of endothelial cells, and vasodilatation of mesenteric arteries. This novel isoform VEGF(165)b is therefore an endogenous inhibitory form of VEGF that is down-regulated in renal tumors and, therefore, may be anti-angiogenesis.

语种: 英语
WOS记录号: WOS:000176871500037
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61537
Appears in Collections:北京大学第一临床医学院_肾脏内科_期刊论文

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作者单位: 1.Univ Bristol, Preclin Vet Sch, Dept Physiol, MIcrovasc Res Labs, Bristol BS2 8EJ, Avon, England
2.Peking Univ, Teaching Hosp 1, Inst Nephrol, Beijing 100871, Peoples R China
3.Southmead Gen Hosp, Bristol Urol Inst, Bristol BS10 5NB, Avon, England
4.Southmead Gen Hosp, Dept Pathol, Bristol BS10 5NB, Avon, England

Recommended Citation:
Bates, DO,Cui, TG,Doughty, JM,et al. VEGF(165)b, an inhibitory splice variant of vascular endothelial growth factor, is down-regulated in renal cell carcinoma[J]. CANCER RESEARCH,2002,62(14):4123-4131.
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