Reversion of deregulated expression of vascular endothelial growth factor in human renal carcinoma cells by von Hippel-Lindau tumor suppressor protein.
Cancer Res
; 56(10): 2299-301, 1996 May 15.
Article
em En
| MEDLINE
| ID: mdl-8625303
ABSTRACT
Mutations or loss of both alleles of the von Hippel-Lindau (VHL) tumor suppressor gene has been documented in sporadic renal cell carcinomas and neoplasms that arise in individuals having the VHL syndrome. The well-vascularized phenotype of tumors that form in VHL disease let us consider vascular endothelial growth factor (VEGF) as a mediator of tumor growth in VHL disease. Human renal carcinoma cells that either lacked endogenous wild-type VHL or were transfected with an inactive mutant VHL showed deregulated expression of VEGF on the mRNA and protein level that was reverted by introduction of wild-type VHL. Stimulation of proliferation of endothelial cells by conditioned medium of cells expressing mutant VHL was almost abolished by neutralizing the VEGF. In contrast, expression of basic fibroblast growth factor and of c-myc proto-oncogene was not affected by VHL. Our data suggest VEGF as the key tumor angiogenesis factor in VHL disease.
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Base de dados:
MEDLINE
Assunto principal:
Carcinoma de Células Renais
/
Proteínas
/
Regulação Neoplásica da Expressão Gênica
/
Fatores de Crescimento Endotelial
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Genes Supressores de Tumor
/
Linfocinas
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Proteínas Supressoras de Tumor
/
Ubiquitina-Proteína Ligases
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Doença de von Hippel-Lindau
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Neoplasias Renais
Limite:
Humans
Idioma:
En
Ano de publicação:
1996
Tipo de documento:
Article