Recombinant adenovirus expressing wild-type p53 is antiagiogenic--implication for lung cancer gene therapy

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6 Citations (Scopus)

Abstract

Angiogenesis is required for the growth and progression of malignancies. Recent studies have demonstrated that genetic alterations may accompany acquisition of the angiogenic phenotype. Here we demonstrate that the recombinant adenovirus-mediated transfer of the wild-type p53 gene into a mutant p53-expressing human non-small cell lung cancer cell line markedly inhibited the expression of an angiogenic factor, vascular endothelial growth factor (VEGF), and increased the expression of a novel antiangiogenic factor, brain-specific angiogenesis inhibitor 1 (BAI 1), resulting in reduced neovascularization in vivo. These results may explain in part the mechanism of the bystander effect induced by wild-type p53 gene transfer of adjacent tumor cells.

Original languageEnglish
Pages (from-to)1217-1224
Number of pages8
JournalGan to kagaku ryoho. Cancer & chemotherapy
Volume27
Issue number8
Publication statusPublished - Jul 2000

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Neoplasm Genes
p53 Genes
Adenoviridae
Genetic Therapy
Lung Neoplasms
Bystander Effect
Angiogenesis Inhibitors
Angiogenesis Inducing Agents
Non-Small Cell Lung Carcinoma
Vascular Endothelial Growth Factor A
Neoplasms
Phenotype
Cell Line
Brain
Growth

ASJC Scopus subject areas

  • Cancer Research
  • Pharmacology

Cite this

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AB - Angiogenesis is required for the growth and progression of malignancies. Recent studies have demonstrated that genetic alterations may accompany acquisition of the angiogenic phenotype. Here we demonstrate that the recombinant adenovirus-mediated transfer of the wild-type p53 gene into a mutant p53-expressing human non-small cell lung cancer cell line markedly inhibited the expression of an angiogenic factor, vascular endothelial growth factor (VEGF), and increased the expression of a novel antiangiogenic factor, brain-specific angiogenesis inhibitor 1 (BAI 1), resulting in reduced neovascularization in vivo. These results may explain in part the mechanism of the bystander effect induced by wild-type p53 gene transfer of adjacent tumor cells.

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