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VEGF(165)b, an inhibitory splice variant of vascular endothelial growth factor, is down-regulated in renal cell carcinoma
Bates, DO; Cui, TG; Doughty, JM; Winkler, M; Sugiono, M; Shields, JD; Peat, D; Gillatt, D; Harper, SJ
刊名CANCER RESEARCH
2002-07-15
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
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被引频次:368[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61537
专题北京大学第一临床医学院_肾脏内科
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
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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.
APA Bates, DO.,Cui, TG.,Doughty, JM.,Winkler, M.,Sugiono, M.,...&Harper, SJ.(2002).VEGF(165)b, an inhibitory splice variant of vascular endothelial growth factor, is down-regulated in renal cell carcinoma.CANCER RESEARCH,62(14),4123-4131.
MLA Bates, DO,et al."VEGF(165)b, an inhibitory splice variant of vascular endothelial growth factor, is down-regulated in renal cell carcinoma".CANCER RESEARCH 62.14(2002):4123-4131.
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