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Resistance of pleural mesothelioma cell lines to apoptosis: relation to expression of Bcl-2 and Bax

Resistance of pleural mesothelioma cell lines to apoptosis: relation to expression of Bcl-2 and Bax 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Lung Cellular and Molecular Physiology The American Physiological Society

Resistance of pleural mesothelioma cell lines to apoptosis: relation to expression of Bcl-2 and Bax

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
1040-0605
eISSN
1522-1504
Publisher site
See Article on Publisher Site

Abstract

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

Journal

AJP - Lung Cellular and Molecular PhysiologyThe American Physiological Society

Published: Jul 1, 1998

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