Protective role of cathepsin L in mouse skin carcinogenesis
Identifieur interne : 001E00 ( Main/Exploration ); précédent : 001D99; suivant : 001E01Protective role of cathepsin L in mouse skin carcinogenesis
Auteurs : Fernando Benavides [États-Unis] ; Carlos Perez [États-Unis] ; Jorge Blando [États-Unis] ; Oscar Contreras [États-Unis] ; Jianjun Shen [États-Unis] ; Lisa M. Coussens [États-Unis] ; Susan M. Fischer [États-Unis] ; Donna F. Kusewitt [États-Unis] ; John Digiovanni [États-Unis] ; Claudio J. Conti [États-Unis]Source :
- Molecular Carcinogenesis [ 0899-1987 ] ; 2012-04.
English descriptors
- Teeft :
- Allele, Anderson cancer center, Basal, Benavides, Body weight, Brdu, Brdu injection, Carcinogenesis, Carcinogenesis protocol, Carcinoma, Cathepsin, Cathepsins, Congenic, Ctsl, Ctsl expression, Ctsl gene, Cysteine, Dmba, Dorsal, Dorsal skin, Epidermal, Epidermal cell proliferation, Epidermal proliferation, Epidermal thickness, Epidermis, Hair follicle morphogenesis, Inbred, Inbred backgrounds, Keratinocyte, Keratinocyte proliferation, Keratinocyte transit, Keratinocytes, Knockout, Knockout mice, Littermate, Littermate controls, Littermates, Lysosomal, Methods section, Molecular carcinogenesis, Mouse, Mouse skin, Mutant, Mutant mice, Mutation, Nackt, Nackt mice, Nackt model, Papilloma, Progression, Proliferation, Protease, Protective role, Skin carcinogenesis, Skin tumorigenesis, Skin tumors, Squamous, Squamous cell carcinomas, Topical applications, Tumor incidence, Tumor multiplicity, Tumor progression, Tumorigenesis, Western blot analysis, Wilcoxon rank.
Abstract
Lysosomal cysteine protease cathepsin L (CTSL) is believed to play a role in tumor progression and is considered a marker for clinically invasive tumors. Studies from our laboratory using the classical mouse skin carcinogenesis model, with 7,12‐dimethyl‐benz[a]anthracene (DMBA) for initiation and 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) for promotion, showed that expression of CTSL is increased in papillomas and squamous cell carcinomas (SCC). We also carried out carcinogenesis studies using Ctsl‐deficient nackt (nkt) mutant mice on three different inbred backgrounds. Unexpectedly, the multiplicity of papillomas was significantly higher in Ctsl‐deficient than in wild‐type mice on two unrelated backgrounds. Topical applications of TPA or DMBA alone to the skin of nkt/nkt mice did not induce papillomas, and there was no increase in spontaneous tumors in nkt/nkt mice on any of the three inbred backgrounds. Reduced epidermal cell proliferation in Ctsl‐deficient nkt/nkt mice after TPA treatment suggested that they are not more sensitive than wild‐type mice to TPA promotion. We also showed that deficiency of CTSL delays terminal differentiation of keratinocytes, and we propose that decreased elimination of initiated cells is at least partially responsible for the increased papilloma formation in the nackt model. Mol. Carcinog. © 2011 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/mc.20792
Affiliations:
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Anderson Cancer Center, Science‐Park, Smithville</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Current Address: Dell Pediatric Research Institute, University of Texas, Austin</wicri:cityArea></affiliation></author><author><name sortKey="Contreras, Oscar" sort="Contreras, Oscar" uniqKey="Contreras O" first="Oscar" last="Contreras">Oscar Contreras</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Department of Molecular Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science‐Park, Smithville</wicri:cityArea></affiliation></author><author><name sortKey="Shen, Jianjun" sort="Shen, Jianjun" uniqKey="Shen J" first="Jianjun" last="Shen">Jianjun Shen</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Department of Molecular Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science‐Park, Smithville</wicri:cityArea></affiliation></author><author><name sortKey="Coussens, Lisa M" sort="Coussens, Lisa M" uniqKey="Coussens L" first="Lisa M." last="Coussens">Lisa M. 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Anderson Cancer Center, Science‐Park, Smithville</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Current Address: Dell Pediatric Research Institute, University of Texas, Austin</wicri:cityArea></affiliation></author><author><name sortKey="Conti, Claudio J" sort="Conti, Claudio J" uniqKey="Conti C" first="Claudio J." last="Conti">Claudio J. Conti</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Department of Molecular Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science‐Park, Smithville</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Molecular Carcinogenesis</title><title level="j" type="alt">MOLECULAR CARCINOGENESIS</title><idno type="ISSN">0899-1987</idno><idno type="eISSN">1098-2744</idno><imprint><biblScope unit="vol">51</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="352">352</biblScope><biblScope unit="page" to="361">361</biblScope><biblScope unit="page-count">10</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-04">2012-04</date></imprint><idno type="ISSN">0899-1987</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0899-1987</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Allele</term><term>Anderson cancer center</term><term>Basal</term><term>Benavides</term><term>Body weight</term><term>Brdu</term><term>Brdu injection</term><term>Carcinogenesis</term><term>Carcinogenesis protocol</term><term>Carcinoma</term><term>Cathepsin</term><term>Cathepsins</term><term>Congenic</term><term>Ctsl</term><term>Ctsl expression</term><term>Ctsl gene</term><term>Cysteine</term><term>Dmba</term><term>Dorsal</term><term>Dorsal skin</term><term>Epidermal</term><term>Epidermal cell proliferation</term><term>Epidermal proliferation</term><term>Epidermal thickness</term><term>Epidermis</term><term>Hair follicle morphogenesis</term><term>Inbred</term><term>Inbred backgrounds</term><term>Keratinocyte</term><term>Keratinocyte proliferation</term><term>Keratinocyte transit</term><term>Keratinocytes</term><term>Knockout</term><term>Knockout mice</term><term>Littermate</term><term>Littermate controls</term><term>Littermates</term><term>Lysosomal</term><term>Methods section</term><term>Molecular carcinogenesis</term><term>Mouse</term><term>Mouse skin</term><term>Mutant</term><term>Mutant mice</term><term>Mutation</term><term>Nackt</term><term>Nackt mice</term><term>Nackt model</term><term>Papilloma</term><term>Progression</term><term>Proliferation</term><term>Protease</term><term>Protective role</term><term>Skin carcinogenesis</term><term>Skin tumorigenesis</term><term>Skin tumors</term><term>Squamous</term><term>Squamous cell carcinomas</term><term>Topical applications</term><term>Tumor incidence</term><term>Tumor multiplicity</term><term>Tumor progression</term><term>Tumorigenesis</term><term>Western blot analysis</term><term>Wilcoxon rank</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lysosomal cysteine protease cathepsin L (CTSL) is believed to play a role in tumor progression and is considered a marker for clinically invasive tumors. Studies from our laboratory using the classical mouse skin carcinogenesis model, with 7,12‐dimethyl‐benz[a]anthracene (DMBA) for initiation and 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) for promotion, showed that expression of CTSL is increased in papillomas and squamous cell carcinomas (SCC). We also carried out carcinogenesis studies using Ctsl‐deficient nackt (nkt) mutant mice on three different inbred backgrounds. Unexpectedly, the multiplicity of papillomas was significantly higher in Ctsl‐deficient than in wild‐type mice on two unrelated backgrounds. Topical applications of TPA or DMBA alone to the skin of nkt/nkt mice did not induce papillomas, and there was no increase in spontaneous tumors in nkt/nkt mice on any of the three inbred backgrounds. Reduced epidermal cell proliferation in Ctsl‐deficient nkt/nkt mice after TPA treatment suggested that they are not more sensitive than wild‐type mice to TPA promotion. We also showed that deficiency of CTSL delays terminal differentiation of keratinocytes, and we propose that decreased elimination of initiated cells is at least partially responsible for the increased papilloma formation in the nackt model. Mol. Carcinog. © 2011 Wiley Periodicals, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>Texas</li></region></list><tree><country name="États-Unis"><region name="Texas"><name sortKey="Benavides, Fernando" sort="Benavides, Fernando" uniqKey="Benavides F" first="Fernando" last="Benavides">Fernando Benavides</name></region><name sortKey="Benavides, Fernando" sort="Benavides, Fernando" uniqKey="Benavides F" first="Fernando" last="Benavides">Fernando Benavides</name><name sortKey="Blando, Jorge" sort="Blando, Jorge" uniqKey="Blando J" first="Jorge" last="Blando">Jorge Blando</name><name sortKey="Blando, Jorge" sort="Blando, Jorge" uniqKey="Blando J" first="Jorge" last="Blando">Jorge Blando</name><name sortKey="Conti, Claudio J" sort="Conti, Claudio J" uniqKey="Conti C" first="Claudio J." last="Conti">Claudio J. Conti</name><name sortKey="Contreras, Oscar" sort="Contreras, Oscar" uniqKey="Contreras O" first="Oscar" last="Contreras">Oscar Contreras</name><name sortKey="Coussens, Lisa M" sort="Coussens, Lisa M" uniqKey="Coussens L" first="Lisa M." last="Coussens">Lisa M. Coussens</name><name sortKey="Digiovanni, John" sort="Digiovanni, John" uniqKey="Digiovanni J" first="John" last="Digiovanni">John Digiovanni</name><name sortKey="Digiovanni, John" sort="Digiovanni, John" uniqKey="Digiovanni J" first="John" last="Digiovanni">John Digiovanni</name><name sortKey="Fischer, Susan M" sort="Fischer, Susan M" uniqKey="Fischer S" first="Susan M." last="Fischer">Susan M. Fischer</name><name sortKey="Kusewitt, Donna F" sort="Kusewitt, Donna F" uniqKey="Kusewitt D" first="Donna F." last="Kusewitt">Donna F. Kusewitt</name><name sortKey="Perez, Carlos" sort="Perez, Carlos" uniqKey="Perez C" first="Carlos" last="Perez">Carlos Perez</name><name sortKey="Shen, Jianjun" sort="Shen, Jianjun" uniqKey="Shen J" first="Jianjun" last="Shen">Jianjun Shen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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