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Abstract A failure of normal apoptosis, often due to mutant p53, may contribute to the formation of a cancer and to its resistance to therapy. Mesothelioma, an asbestos-induced tumor, is highly resistant to therapy but generally expresses wild-type p53. We asked whether mesothelioma was resistant to apoptosis and whether resistance was associated with altered expression of the antiapoptotic protein Bcl-2 or proapoptotic protein Bax. We found that three mesothelioma cell lines (1 with wild-type p53) were highly resistant to apoptosis induced by oxidant stimuli (asbestos, H 2 O 2 ) or nonoxidant stimuli (calcium ionophore) compared with primary cultured mesothelial cells. By immunostaining, one of these three lines expressed Bcl-2 but only during mitosis. By immunoblotting, 3 of 14 additional mesothelioma lines (9 of 14 with wild type p53) expressed Bcl-2 but all 14 of 14 expressed the proapoptotic Bax, giving a low ratio of Bcl-2 to Bax. We conclude that mesothelioma cell lines are resistant to apoptosis and that the failure in apoptosis is not explained by Bcl-2 but by other mechanisms that counteract the proapoptotic effect of Bax. mesothelial cell p53 reactive oxygen species asbestos cancer Footnotes Address for reprint requests: V. C. Broaddus, Lung Biology Center, Box 0854, Univ. of California, San Francisco, CA 94143-0854. S. R. Narasimhan and V. C. Broaddus were supported by National Institute of Environmental Health Sciences Grants ES-06331 and ES-08985 and by an Academic Senate Award. Copyright © 1998 the American Physiological Society
AJP - Lung Cellular and Molecular Physiology – The American Physiological Society
Published: Jul 1, 1998
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