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Clinical Cancer Research Vol. 5, 1015-1023, May 1999
© 1999 American Association for Cancer Research

Advances in Brief

Recombinant Adenovirus Expressing Wild-Type p53 Is Antiangiogenic: A Proposed Mechanism for Bystander Effect1

Masahiko Nishizaki, Toshiyoshi Fujiwara2, Tohru Tanida, Akio Hizuta, Hiroyuki Nishimori, Takashi Tokino, Yusuke Nakamura, Michael Bouvet, Jack A. Roth and Noriaki Tanaka

Section of Molecular Oncology [M. N., T. F., T. Ta.] and First Department of Surgery [A. H., N. T.], Okayama University Medical School, Okayama 700-8558, Japan; Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [H. N., T. To., Y. N.]; and Section of Thoracic Molecular Oncology, Department of Thoracic and Cardiovascular Surgery, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030 [M. B., J. A. R.]

Angiogenesis is required for the growth and progression of malignancies. Recent studies have demonstrated that genetic alterations may accompany acquisition of the angiogenic phenotype. The tumor suppressor gene p53 is most frequently mutated in human cancers and is also known to be a transcriptional regulator of a variety of genes. Here, we investigated the antiangiogenic effect of the wild-type p53 (wt-p53) gene transfer on a human non-small cell lung cancer cell line. Mutant p53-expressing H226Br non-small cell lung cancer cells were transduced with the wt-p53 gene using a recombinant adenoviral vector (Ad5CMVp53) and applied to semiquantitative reverse transcription-PCRs for the detection of altered mRNA expression of angiogenic and/or antiangiogenic factors. In vivo neovascularization assay of Ad5CMVp53-infected cells was then performed using a membrane-diffusion chamber system s.c. transplanted in nu/nu mice. We also evaluated the effect of Ad5CMVp53-infected H226Br cells on nontransduced tumor cells in vivo by s.c. inoculating mixture of cells into nu/nu mice. Ad5CMVp53 infection markedly inhibited the expression of an angiogenic factor, vascular endothelial growth factor, and increased the expression of a novel antiangiogenic factor, brain-specific angiogenesis inhibitor 1, resulting in reduced neovascularization in vivo. Mixing experiments showed that tumor cells transduced with the wt-p53 gene inhibited the in vivo tumor growth of adjacent nontransduced cells. Our data suggest that a recombinant adenovirus expressing the wt-p53 gene is antiangiogenic, which may explain, in part, the mechanism of the bystander effect induced by the wt-p53 gene transfer on adjacent tumor cells.




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