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Clinical Cancer Research Vol. 6, 887-890, March 2000
© 2000 American Association for Cancer Research

Experimental Therapeutics, Preclinical Pharmacology

Up-Regulation of the Proapoptotic Mediators Bax and Bak after Adenovirus-mediated p53 Gene Transfer in Lung Cancer Cells1

A. Scott Pearson2, Francis R. Spitz2, Stephen G. Swisher3, Masafumi Kataoka, Mona G. Sarkiss, Raymond E. Meyn, Timothy J. McDonnell, Richard J. Cristiano and Jack A. Roth

Departments of Surgical Oncology [A. S. P., F. R. S.], Experimental Radiation Oncology [R. E. M.], Molecular Pathology [T. J. M., M. G. S.], and Section of Thoracic Molecular Oncology, Department of Thoracic and Cardiovascular Surgery [S. G. S., M. K., R. J. C., J. A. R.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Overexpression of wild-type p53 in cancer cells by adenovirus-mediated p53 gene transfer can result in the induction of apoptosis. To identify the potential mediators of this p53-induced apoptosis, we examined apoptotic protein levels in human lung cancer cells after Adp53 gene transfer. We observed up-regulation of Bax and Bak protein levels 18–36 h after transduction with Adp53 in H1299, H358, and H322 lung cancer cells. Contrary to expected observations, no changes in Bcl-2 and Bcl-XL protein levels were observed. Morphological cell changes and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining showed evidence of apoptosis in all cell lines 48 h after transduction with Adp53. These results indicate that the induction of apoptosis by adenovirus-mediated p53 transfer may be mediated by the induction of proapoptotic mechanisms rather than suppression of antiapoptotic mechanisms.




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