p53Protein expression is correlated with benzo[a]pyrene-DNA adducts in carcinoma cell lines
Identifieur interne : 002645 ( Istex/Corpus ); précédent : 002644; suivant : 002646p53Protein expression is correlated with benzo[a]pyrene-DNA adducts in carcinoma cell lines
Auteurs : Mika R Met ; Katariina Castrén ; Kaisu J Rvinen ; Katja Pekkala ; Taina Turpeenniemi-Hujanen ; Ylermi Soini ; Paavo P Kkö ; Kirsi V H KangasSource :
- Carcinogenesis [ 0143-3334 ] ; 1995-09.
Abstract
p53 inhibits cell cycle progression and DNA damaging cytostatics induce p53 protein expression, indicating that p53 responds to DNA damage. We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression. The most relevant DNA adducts for carcinogenesis, benzo[a]pyrene-7,8-diol-9,10-epoxide-DNA adducts, were measured by synchronous fluorescence spectrophotometry and p53 immunohistochemistry using polyclonal antibody CM1, which detects both wild-type and mutated forms of p53. Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression. α-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response. The cell lines not able to activate BP, A-427 and SK-LU-1 (both human lung carcinomas), SK-MES-1 (human lung squamous carcinoma) and human fibroblasts, did not show any increase in p53 immunohistochemistry. The OVCAR-3 ovarian adenocarcinoma cell line, containing a mutation in exon 7 of p53, and the SK-LU-1 cell line expressed very high levels of p53 protein before BP treatment and no increase in p53 immunohistochemistry was seen. These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.
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DOI: 10.1093/carcin/16.9.2117
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Central University Hospital Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="Pekkala, Katja" sort="Pekkala, Katja" uniqKey="Pekkala K" first="Katja" last="Pekkala">Katja Pekkala</name><affiliation><mods:affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="Turpeenniemi Hujanen, Taina" sort="Turpeenniemi Hujanen, Taina" uniqKey="Turpeenniemi Hujanen T" first="Taina" last="Turpeenniemi-Hujanen">Taina Turpeenniemi-Hujanen</name><affiliation><mods:affiliation>Department of Oncology, Central University Hospital Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="Soini, Ylermi" sort="Soini, Ylermi" uniqKey="Soini Y" first="Ylermi" last="Soini">Ylermi Soini</name><affiliation><mods:affiliation>Department of Pathology, University of Oulu Oulu, Finland</mods:affiliation></affiliation></author><author><name 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Rvinen</name><affiliation><mods:affiliation>Department of Oncology, Central University Hospital Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="Pekkala, Katja" sort="Pekkala, Katja" uniqKey="Pekkala K" first="Katja" last="Pekkala">Katja Pekkala</name><affiliation><mods:affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="Turpeenniemi Hujanen, Taina" sort="Turpeenniemi Hujanen, Taina" uniqKey="Turpeenniemi Hujanen T" first="Taina" last="Turpeenniemi-Hujanen">Taina Turpeenniemi-Hujanen</name><affiliation><mods:affiliation>Department of Oncology, Central University Hospital Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="Soini, Ylermi" sort="Soini, Ylermi" uniqKey="Soini Y" first="Ylermi" last="Soini">Ylermi Soini</name><affiliation><mods:affiliation>Department of Pathology, University of Oulu Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="P Kko, Paavo" sort="P Kko, Paavo" uniqKey="P Kko P" first="Paavo" last="P Kkö">Paavo P Kkö</name><affiliation><mods:affiliation>Department of Pathology, University of Oulu Oulu, Finland</mods:affiliation></affiliation></author><author><name sortKey="V H Kangas, Kirsi" sort="V H Kangas, Kirsi" uniqKey="V H Kangas K" first="Kirsi" last="V H Kangas">Kirsi V H Kangas</name><affiliation><mods:affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</mods:affiliation></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="1995-09">1995-09</date><biblScope unit="volume">16</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" 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We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression. The most relevant DNA adducts for carcinogenesis, benzo[a]pyrene-7,8-diol-9,10-epoxide-DNA adducts, were measured by synchronous fluorescence spectrophotometry and p53 immunohistochemistry using polyclonal antibody CM1, which detects both wild-type and mutated forms of p53. Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression. α-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response. The cell lines not able to activate BP, A-427 and SK-LU-1 (both human lung carcinomas), SK-MES-1 (human lung squamous carcinoma) and human fibroblasts, did not show any increase in p53 immunohistochemistry. The OVCAR-3 ovarian adenocarcinoma cell line, containing a mutation in exon 7 of p53, and the SK-LU-1 cell line expressed very high levels of p53 protein before BP treatment and no increase in p53 immunohistochemistry was seen. These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Mika Rämet</name><affiliations><json:string>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</json:string></affiliations></json:item><json:item><name>Katariina Castrén</name><affiliations><json:string>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</json:string></affiliations></json:item><json:item><name>Kaisu Järvinen</name><affiliations><json:string>Department of Oncology, Central University Hospital Oulu, Finland</json:string></affiliations></json:item><json:item><name>Katja Pekkala</name><affiliations><json:string>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</json:string></affiliations></json:item><json:item><name>Taina Turpeenniemi-Hujanen</name><affiliations><json:string>Department of Oncology, Central University Hospital Oulu, Finland</json:string></affiliations></json:item><json:item><name>Ylermi Soini</name><affiliations><json:string>Department of Pathology, University of Oulu Oulu, Finland</json:string></affiliations></json:item><json:item><name>Paavo Pääkkö</name><affiliations><json:string>Department of Pathology, University of Oulu Oulu, Finland</json:string></affiliations></json:item><json:item><name>Kirsi Vähäkangas</name><affiliations><json:string>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>ORIGINAL ARTICLES</value></json:item></subject><articleId><json:string>16.9.2117</json:string></articleId><language><json:string>eng</json:string></language><abstract>p53 inhibits cell cycle progression and DNA damaging cytostatics induce p53 protein expression, indicating that p53 responds to DNA damage. We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression. The most relevant DNA adducts for carcinogenesis, benzo[a]pyrene-7,8-diol-9,10-epoxide-DNA adducts, were measured by synchronous fluorescence spectrophotometry and p53 immunohistochemistry using polyclonal antibody CM1, which detects both wild-type and mutated forms of p53. Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression. α-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response. The cell lines not able to activate BP, A-427 and SK-LU-1 (both human lung carcinomas), SK-MES-1 (human lung squamous carcinoma) and human fibroblasts, did not show any increase in p53 immunohistochemistry. The OVCAR-3 ovarian adenocarcinoma cell line, containing a mutation in exon 7 of p53, and the SK-LU-1 cell line expressed very high levels of p53 protein before BP treatment and no increase in p53 immunohistochemistry was seen. These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.</abstract><qualityIndicators><score>7.304</score><pdfVersion>1.2</pdfVersion><pdfPageSize>605 x 802 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>1347</abstractCharCount><pdfWordCount>5011</pdfWordCount><pdfCharCount>31218</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>192</abstractWordCount></qualityIndicators><title>p53Protein expression is correlated with benzo[a]pyrene-DNA adducts in carcinoma cell 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type="first">Taina</forename><surname>Turpeenniemi-Hujanen</surname></persName><affiliation>Department of Oncology, Central University Hospital Oulu, Finland</affiliation></author><author><persName><forename type="first">Ylermi</forename><surname>Soini</surname></persName><affiliation>Department of Pathology, University of Oulu Oulu, Finland</affiliation></author><author><persName><forename type="first">Paavo</forename><surname>Pääkkö</surname></persName><affiliation>Department of Pathology, University of Oulu Oulu, Finland</affiliation></author><author><persName><forename type="first">Kirsi</forename><surname>Vähäkangas</surname></persName><affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</affiliation></author></analytic><monogr><title level="j">Carcinogenesis</title><idno type="pISSN">0143-3334</idno><idno type="eISSN">1460-2180</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1995-09"></date><biblScope unit="volume">16</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="2117">2117</biblScope><biblScope unit="page" to="2124">2124</biblScope></imprint></monogr><idno type="istex">60D6EFB4BFED60C8F3EA7E03AD5D1B01E2CBC67D</idno><idno type="DOI">10.1093/carcin/16.9.2117</idno><idno type="ArticleID">16.9.2117</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>p53 inhibits cell cycle progression and DNA damaging cytostatics induce p53 protein expression, indicating that p53 responds to DNA damage. We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression. The most relevant DNA adducts for carcinogenesis, benzo[a]pyrene-7,8-diol-9,10-epoxide-DNA adducts, were measured by synchronous fluorescence spectrophotometry and p53 immunohistochemistry using polyclonal antibody CM1, which detects both wild-type and mutated forms of p53. Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression. α-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response. The cell lines not able to activate BP, A-427 and SK-LU-1 (both human lung carcinomas), SK-MES-1 (human lung squamous carcinoma) and human fibroblasts, did not show any increase in p53 immunohistochemistry. The OVCAR-3 ovarian adenocarcinoma cell line, containing a mutation in exon 7 of p53, and the SK-LU-1 cell line expressed very high levels of p53 protein before BP treatment and no increase in p53 immunohistochemistry was seen. These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>ORIGINAL ARTICLES</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-09">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-15">References added</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-21">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/60D6EFB4BFED60C8F3EA7E03AD5D1B01E2CBC67D/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">carcin</journal-id><journal-id journal-id-type="publisher-id">carcin</journal-id><journal-id journal-id-type="pmc">carcin</journal-id><journal-title>Carcinogenesis</journal-title><issn pub-type="epub">1460-2180</issn><issn pub-type="ppub">0143-3334</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/carcin/16.9.2117</article-id><article-id pub-id-type="publisher-id">16.9.2117</article-id><article-categories><subj-group><subject>ORIGINAL ARTICLES</subject></subj-group></article-categories><title-group><article-title>p<sup>53</sup>Protein expression is correlated with benzo[<italic>a</italic>]pyrene-DNA adducts in carcinoma cell lines</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Rämet</surname><given-names>Mika</given-names></name></contrib><contrib contrib-type="author"><name><surname>Castrén</surname><given-names>Katariina</given-names></name></contrib><contrib contrib-type="author"><name><surname>Järvinen</surname><given-names>Kaisu</given-names></name><xref ref-type="aff" rid="au1"></xref></contrib><contrib contrib-type="author"><name><surname>Pekkala</surname><given-names>Katja</given-names></name></contrib><contrib contrib-type="author"><name><surname>Turpeenniemi-Hujanen</surname><given-names>Taina</given-names></name><xref ref-type="aff" rid="au1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Soini</surname><given-names>Ylermi</given-names></name><xref ref-type="aff" rid="au2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Pääkkö</surname><given-names>Paavo</given-names></name><xref ref-type="aff" rid="au2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Vähäkangas</surname><given-names>Kirsi</given-names></name><xref ref-type="corresp" rid="cor1"><sup>3</sup></xref></contrib><aff><institution>Department of Pharmacology and Toxicology, University of Oulu</institution> <addr-line>Oulu, Finland</addr-line></aff><aff id="au1"><sup>1</sup><institution>Department of Oncology, Central University Hospital</institution> <addr-line>Oulu, Finland</addr-line></aff><aff id="au2"><sup>2</sup><institution>Department of Pathology, University of Oulu</institution> <addr-line>Oulu, Finland</addr-line></aff></contrib-group><author-notes><corresp id="cor1"><sup>3</sup>To whom correspondence should be addressed</corresp></author-notes><pub-date pub-type="ppub"><month>9</month><year>1995</year></pub-date><volume>16</volume><issue>9</issue><fpage>2117</fpage><lpage>2124</lpage><history><date date-type="received"><day>04</day><month>4</month><year>1995</year></date><date date-type="rev-recd"><day>07</day><month>6</month><year>1995</year></date><date date-type="accepted"><day>07</day><month>6</month><year>1995</year></date></history><copyright-statement>© Oxford University Press</copyright-statement><copyright-year>1995</copyright-year><abstract><p>p53 inhibits cell cycle progression and DNA damaging cytostatics induce p53 protein expression, indicating that p53 responds to DNA damage. We have measured benzo[<italic>a</italic>]pyrene (BP)-induced DNA damage in association with p53 expression. The most relevant DNA adducts for carcinogenesis, benzo[<italic>a</italic>]pyrene-7,8-diol-9,10-epoxide-DNA adducts, were measured by synchronous fluorescence spectrophotometry and p53 immunohistochemistry using polyclonal antibody CM1, which detects both wild-type and mutated forms of p53. Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression. α-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response. The cell lines not able to activate BP, A-427 and SK-LU-1 (both human lung carcinomas), SK-MES-1 (human lung squamous carcinoma) and human fibroblasts, did not show any increase in p53 immunohistochemistry. The OVCAR-3 ovarian adenocarcinoma cell line, containing a mutation in exon 7 of <italic>p</italic>53, and the SK-LU-1 cell line expressed very high levels of p53 protein before BP treatment and no increase in p53 immunohistochemistry was seen. These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>p53Protein expression is correlated with benzo[a]pyrene-DNA adducts in carcinoma cell lines</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>p53Protein expression is correlated with benzo[a]pyrene-DNA adducts in carcinoma cell lines</title></titleInfo><name type="personal"><namePart type="given">Mika</namePart><namePart type="family">Rämet</namePart><affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katariina</namePart><namePart type="family">Castrén</namePart><affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kaisu</namePart><namePart type="family">Järvinen</namePart><affiliation>Department of Oncology, Central University Hospital Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katja</namePart><namePart type="family">Pekkala</namePart><affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Taina</namePart><namePart type="family">Turpeenniemi-Hujanen</namePart><affiliation>Department of Oncology, Central University Hospital Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ylermi</namePart><namePart type="family">Soini</namePart><affiliation>Department of Pathology, University of Oulu Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paavo</namePart><namePart type="family">Pääkkö</namePart><affiliation>Department of Pathology, University of Oulu Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kirsi</namePart><namePart type="family">Vähäkangas</namePart><affiliation>Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland, Oulu, Finland, Oulu, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>ORIGINAL ARTICLES</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1995-09</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>p53 inhibits cell cycle progression and DNA damaging cytostatics induce p53 protein expression, indicating that p53 responds to DNA damage. We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression. The most relevant DNA adducts for carcinogenesis, benzo[a]pyrene-7,8-diol-9,10-epoxide-DNA adducts, were measured by synchronous fluorescence spectrophotometry and p53 immunohistochemistry using polyclonal antibody CM1, which detects both wild-type and mutated forms of p53. Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression. α-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response. The cell lines not able to activate BP, A-427 and SK-LU-1 (both human lung carcinomas), SK-MES-1 (human lung squamous carcinoma) and human fibroblasts, did not show any increase in p53 immunohistochemistry. The OVCAR-3 ovarian adenocarcinoma cell line, containing a mutation in exon 7 of p53, and the SK-LU-1 cell line expressed very high levels of p53 protein before BP treatment and no increase in p53 immunohistochemistry was seen. These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.</abstract><note type="author-notes">3To whom correspondence should be addressed</note><relatedItem type="host"><titleInfo><title>Carcinogenesis</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0143-3334</identifier><identifier type="eISSN">1460-2180</identifier><identifier type="PublisherID">carcin</identifier><identifier type="PublisherID-hwp">carcin</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>2117</start><end>2124</end></extent></part></relatedItem><identifier type="istex">60D6EFB4BFED60C8F3EA7E03AD5D1B01E2CBC67D</identifier><identifier type="DOI">10.1093/carcin/16.9.2117</identifier><identifier type="ArticleID">16.9.2117</identifier><accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/60D6EFB4BFED60C8F3EA7E03AD5D1B01E2CBC67D/annexes/pdf</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/60D6EFB4BFED60C8F3EA7E03AD5D1B01E2CBC67D/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">ONCOLOGY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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