Human mesothelioma cells and asbestos-exposed mesothelial cells are selectively resistant to amosite toxicity: a possible mechanism for tumor promotion by asbestos
Identifieur interne : 00DA89 ( Main/Exploration ); précédent : 00DA88; suivant : 00DA90Human mesothelioma cells and asbestos-exposed mesothelial cells are selectively resistant to amosite toxicity: a possible mechanism for tumor promotion by asbestos
Auteurs : Edward W. Gabrielson [États-Unis] ; Anne Van Der Meeren [États-Unis, France] ; Roger R. Reddel [États-Unis, Australie] ; Helen Reddel [États-Unis, Australie] ; Brenda I. Gerwin [États-Unis] ; Curtis C. Harris [États-Unis]Source :
- Carcinogenesis [ 0143-3334 ] ; 1992-08.
Abstract
To determine if asbestos exposure could contribute to mesothelial cell carcinogenesis by selection and/or expansion of an initiated cell population, we compared normal human pleural mesothelial cells to either human mesothelioma cell lines or mesothelial cells transfected with cancer-related genes for sensitivity to amosite fibers in vitro. Neither normal nor mesothelioma cells were directly stimulated to replicate or increase DNA synthesis by any of the asbestos exposure conditions tested. The potential selective effect of asbestos exposure was demonstrated by a differential sensitivity of normal mesothelial cells and mesothelioma cells to amosite: for example, up to 20-fold higher concentrations of amosite fibers were required to inhibit replication of mesothelioma cell lines than normal mesothelial cells. In addition, a significant resistance (4-fold) to amosite toxicity was observed for SV40 immortalized mesothelial cell lines that had previously been selected in vitro for resistance to asbestos. SV40 immortalized cells that have become tumorigenic after transfection with either Ha-ras or PDGF A-chain genes were not significantly more resistant to the cytotoxic effects of amosite than primary normal cells, and the primary cells were equally sensitive to amosite as mesothelial cells that were only immortalized by SV40. The sensitivity of normal mesothelial cells to asbestos does not appear to be simply a result of general fragility of the mesothelial cells, since similar levels of hydrogen peroxide and silica were cytotoxic for normal mesothelial cells and mesothelioma cell lines. Because mesothelioma cells have a greater resistance to asbestos cytotoxkity than normal mesothelial cells, we hypothesize that a differential resistance to cell killing by asbestos fibers in vitro may result in a selective expansion of an initiated or transformed cell population and thus contribute to the carcinogenesis process. Since tumorigenicity and asbestos resistance occur independently of one another in genetically altered mesothelial cell lines, genotypic and phenotypic alterations that lead to tumorigenic conversion may not be the same changes that provide resistance to cell killing by asbestos.
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DOI: 10.1093/carcin/13.8.1359
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Reddel</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Human Carcinogenesis, Division of Cancer Etiology, National Cancer Institute Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Present address: Children's Medical Research Foundation, PO Box 61, Camperdown, NSW 2050</wicri:regionArea><wicri:noRegion>NSW 2050</wicri:noRegion></affiliation></author><author><name sortKey="Reddel, Helen" sort="Reddel, Helen" uniqKey="Reddel H" first="Helen" last="Reddel">Helen Reddel</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Human Carcinogenesis, Division of Cancer Etiology, National Cancer Institute Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">Australie</country><wicri:regionArea>Present address: Department of Respiratory Medicine, Blackburn Building D06, University of Sydney, NSW 2006</wicri:regionArea><orgName type="university">Université de Sydney</orgName><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation></author><author><name sortKey="Gerwin, Brenda I" sort="Gerwin, Brenda I" uniqKey="Gerwin B" first="Brenda I." last="Gerwin">Brenda I. 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Harris</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Human Carcinogenesis, Division of Cancer Etiology, National Cancer Institute Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Carcinogenesis</title><idno type="ISSN">0143-3334</idno><idno type="eISSN">1460-2180</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1992-08">1992-08</date><biblScope unit="volume">13</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1359">1359</biblScope><biblScope unit="page" to="1363">1363</biblScope></imprint><idno type="ISSN">0143-3334</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0143-3334</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">To determine if asbestos exposure could contribute to mesothelial cell carcinogenesis by selection and/or expansion of an initiated cell population, we compared normal human pleural mesothelial cells to either human mesothelioma cell lines or mesothelial cells transfected with cancer-related genes for sensitivity to amosite fibers in vitro. Neither normal nor mesothelioma cells were directly stimulated to replicate or increase DNA synthesis by any of the asbestos exposure conditions tested. The potential selective effect of asbestos exposure was demonstrated by a differential sensitivity of normal mesothelial cells and mesothelioma cells to amosite: for example, up to 20-fold higher concentrations of amosite fibers were required to inhibit replication of mesothelioma cell lines than normal mesothelial cells. In addition, a significant resistance (4-fold) to amosite toxicity was observed for SV40 immortalized mesothelial cell lines that had previously been selected in vitro for resistance to asbestos. SV40 immortalized cells that have become tumorigenic after transfection with either Ha-ras or PDGF A-chain genes were not significantly more resistant to the cytotoxic effects of amosite than primary normal cells, and the primary cells were equally sensitive to amosite as mesothelial cells that were only immortalized by SV40. The sensitivity of normal mesothelial cells to asbestos does not appear to be simply a result of general fragility of the mesothelial cells, since similar levels of hydrogen peroxide and silica were cytotoxic for normal mesothelial cells and mesothelioma cell lines. Because mesothelioma cells have a greater resistance to asbestos cytotoxkity than normal mesothelial cells, we hypothesize that a differential resistance to cell killing by asbestos fibers in vitro may result in a selective expansion of an initiated or transformed cell population and thus contribute to the carcinogenesis process. Since tumorigenicity and asbestos resistance occur independently of one another in genetically altered mesothelial cell lines, genotypic and phenotypic alterations that lead to tumorigenic conversion may not be the same changes that provide resistance to cell killing by asbestos.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li><li>États-Unis</li></country><region><li>Maryland</li><li>Nouvelle-Galles du Sud</li></region><settlement><li>Sydney</li></settlement><orgName><li>Université de Sydney</li></orgName></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Gabrielson, Edward W" sort="Gabrielson, Edward W" uniqKey="Gabrielson E" first="Edward W." last="Gabrielson">Edward W. Gabrielson</name></region><name sortKey="Der Meeren, Anne Van" sort="Der Meeren, Anne Van" uniqKey="Der Meeren A" first="Anne Van" last="Der Meeren">Anne Van Der Meeren</name><name sortKey="Gabrielson, Edward W" sort="Gabrielson, Edward W" uniqKey="Gabrielson E" first="Edward W." last="Gabrielson">Edward W. Gabrielson</name><name sortKey="Gabrielson, Edward W" sort="Gabrielson, Edward W" uniqKey="Gabrielson E" first="Edward W." last="Gabrielson">Edward W. Gabrielson</name><name sortKey="Gerwin, Brenda I" sort="Gerwin, Brenda I" uniqKey="Gerwin B" first="Brenda I." last="Gerwin">Brenda I. Gerwin</name><name sortKey="Harris, Curtis C" sort="Harris, Curtis C" uniqKey="Harris C" first="Curtis C." last="Harris">Curtis C. Harris</name><name sortKey="Reddel, Helen" sort="Reddel, Helen" uniqKey="Reddel H" first="Helen" last="Reddel">Helen Reddel</name><name sortKey="Reddel, Roger R" sort="Reddel, Roger R" uniqKey="Reddel R" first="Roger R." last="Reddel">Roger R. Reddel</name></country><country name="France"><noRegion><name sortKey="Der Meeren, Anne Van" sort="Der Meeren, Anne Van" uniqKey="Der Meeren A" first="Anne Van" last="Der Meeren">Anne Van Der Meeren</name></noRegion></country><country name="Australie"><noRegion><name sortKey="Reddel, Roger R" sort="Reddel, Roger R" uniqKey="Reddel R" first="Roger R." last="Reddel">Roger R. Reddel</name></noRegion><name sortKey="Reddel, Helen" sort="Reddel, Helen" uniqKey="Reddel H" first="Helen" last="Reddel">Helen Reddel</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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