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JNCI Journal of the National Cancer Institute 2000 92(8):636-641; doi:10.1093/jnci/92.8.636
© 2000 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 92, No. 8, 636-641, April 19, 2000
© 2000 Oxford University Press

Adenovirus-Mediated p14ARF Gene Transfer in Human Mesothelioma Cells

Cheng-Ta Yang, Liang You, Che-Chung Yeh, John Wen-Cheng Chang, Fen Zhang, Frank McCormick, David M. Jablons

Affiliations of authors: C.-T. Yang, Thoracic Oncology Laboratory, University of California, San Francisco Cancer Center, and Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan; L. You, F. McCormick, D. M. Jablons (Thoracic Oncology Laboratory), C.-C. Yeh (Molecular Urology Laboratory), J. W.-C. Chang (Department of Surgery), F. Zhang (Department of Ophthalmology), University of California, San Francisco.

Correspondence to: David M. Jablons, M.D., Section of General Thoracic Surgery, University of California, San Francisco, Campus Box 1674, San Francisco, CA 94115 (e-mail: jablonsd{at}surgery.ucsf.edu).

Background: The p14ARF protein encoded by the INK4a/ARF locus promotes degradation of the MDM2 protein and thus prevents the MDM2-mediated inhibition of p53. Homozygous deletion of the INK4a/ARF locus is common in human mesothelioma and may result in the loss of p14ARF and the inactivation of p53. We designed this study to evaluate the biologic and potential therapeutic roles of p14ARF expression in mesothelioma cells. Methods and Results: We constructed Adp14, an adenoviral vector carrying human p14ARF complementary DNA, and used it to transfect human mesothelioma cell lines H28, H513, H2052, and MSTO-211H. Overexpression of p14ARF led to increased amounts of p53 and the p21WAF proteins and dephosphorylation of the retinoblastoma protein. The growth rate of mesothelioma cells was inhibited markedly by infection with Adp14 compared with mock infection or infection with a control adenovirus vector, AdCtrl. Overexpression of p14ARF induced G1-phase cell cycle arrest and apoptotic cell death. Cytotoxicity assays showed that Adp14 had a statistically significantly (P = .002) greater effect on colon cancer (HCT116) cell lines containing two copies of the wild-type p53 gene than on p53-null cells, suggesting that functional p53 is a critical determinant of p14ARF-mediated cytotoxicity. Conclusions: The transfection of p14ARF into mesothelioma cells led to the overexpression of p14ARF, which resulted in G1-phase arrest and apoptotic cell death. These results suggest that this gene therapy-based approach may be of use in the treatment of mesothelioma.


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