Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions
Autor(a) principal: | |
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Data de Publicação: | 2012 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/34339 http://dx.doi.org/10.1016/j.canlet.2011.09.019 |
Resumo: | Doxorubicin (DOX) is an important tumor chemotherapeutic agent, acting mainly by genotoxic action. This work focus on cell processes that help cell survival, after DOX-induced DNA damage. in fact, cells deficient for XPA or DNA polymerase eta (pol eta, XPV) proteins (involved in distinct DNA repair pathways) are highly DOX-sensitive. Moreover, LY294002, an inhibitor of PIKK kinases, showed a synergistic killing effect in cells deficient in these proteins, with a strong induction of G2/M cell cycle arrest. Taken together, these results indicate that XPA and pol eta proteins participate in cell resistance to DOX-treatment, and kinase inhibitors can selectively enhance its killing effects, probably reducing the cell ability to recover from breaks induced in DNA. (C) 2011 Elsevier Ireland Ltd. All rights reserved. |
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Moraes, Maria Carolina S.Andrade, Annabel Quinet deCarvalho, Helotonio [UNIFESP]Guecheva, TemenougaAgnoletto, Mateus H.Henriques, Joao A. P.Sarasin, AlainStary, AnneSaffi, JeniferMenck, Carlos F. M.Universidade de São Paulo (USP)Univ Paris SudUniversidade Federal de São Paulo (UNIFESP)Univ Fed Rio Grande do SulFed Univ Hlth Sci Porto Alegre UFCSPA2016-01-24T14:17:35Z2016-01-24T14:17:35Z2012-01-01Cancer Letters. Clare: Elsevier B.V., v. 314, n. 1, p. 108-118, 2012.0304-3835http://repositorio.unifesp.br/handle/11600/34339http://dx.doi.org/10.1016/j.canlet.2011.09.019WOS000298531900012.pdf10.1016/j.canlet.2011.09.019WOS:000298531900012Doxorubicin (DOX) is an important tumor chemotherapeutic agent, acting mainly by genotoxic action. This work focus on cell processes that help cell survival, after DOX-induced DNA damage. in fact, cells deficient for XPA or DNA polymerase eta (pol eta, XPV) proteins (involved in distinct DNA repair pathways) are highly DOX-sensitive. Moreover, LY294002, an inhibitor of PIKK kinases, showed a synergistic killing effect in cells deficient in these proteins, with a strong induction of G2/M cell cycle arrest. Taken together, these results indicate that XPA and pol eta proteins participate in cell resistance to DOX-treatment, and kinase inhibitors can selectively enhance its killing effects, probably reducing the cell ability to recover from breaks induced in DNA. (C) 2011 Elsevier Ireland Ltd. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)USP-COFECUB (São Paulo, Brazil)Univ São Paulo, Dept Microbiol, Inst Biomed Sci, São Paulo, BrazilUniv Paris Sud, Inst Gustave Roussy, Ctr Natl Rech Sci, UMR8200, Villejuif, FranceFed Univ São Paulo UNIFESP, Dept Biol Sci, Diadema, SP, BrazilUniv Fed Rio Grande do Sul, Ctr Biotechnol, Dept Biophys, Porto Alegre, RS, BrazilFed Univ Hlth Sci Porto Alegre UFCSPA, Dept Basic Hlth Sci, Porto Alegre, RS, BrazilFed Univ São Paulo UNIFESP, Dept Biol Sci, Diadema, SP, BrazilWeb of Science108-118engElsevier B.V.Cancer Lettershttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policyinfo:eu-repo/semantics/openAccessDoxorubicinDNA polymerase eta (pol eta)XPVXPALY294002DNA repairBoth XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesionsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000298531900012.pdfapplication/pdf1786229${dspace.ui.url}/bitstream/11600/34339/1/WOS000298531900012.pdfff5701507e1074499fbb33b43f9891adMD51open accessTEXTWOS000298531900012.pdf.txtWOS000298531900012.pdf.txtExtracted texttext/plain41771${dspace.ui.url}/bitstream/11600/34339/9/WOS000298531900012.pdf.txt8ddaa766344acf6b4e0180e657f059c6MD59open accessTHUMBNAILWOS000298531900012.pdf.jpgWOS000298531900012.pdf.jpgIM Thumbnailimage/jpeg6847${dspace.ui.url}/bitstream/11600/34339/11/WOS000298531900012.pdf.jpge8523382b4caa2c9746059f469bc96ccMD511open access11600/343392023-06-05 19:33:22.256open accessoai:repositorio.unifesp.br:11600/34339Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-06-05T22:33:22Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
title |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
spellingShingle |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions Moraes, Maria Carolina S. Doxorubicin DNA polymerase eta (pol eta) XPV XPA LY294002 DNA repair |
title_short |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
title_full |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
title_fullStr |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
title_full_unstemmed |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
title_sort |
Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions |
author |
Moraes, Maria Carolina S. |
author_facet |
Moraes, Maria Carolina S. Andrade, Annabel Quinet de Carvalho, Helotonio [UNIFESP] Guecheva, Temenouga Agnoletto, Mateus H. Henriques, Joao A. P. Sarasin, Alain Stary, Anne Saffi, Jenifer Menck, Carlos F. M. |
author_role |
author |
author2 |
Andrade, Annabel Quinet de Carvalho, Helotonio [UNIFESP] Guecheva, Temenouga Agnoletto, Mateus H. Henriques, Joao A. P. Sarasin, Alain Stary, Anne Saffi, Jenifer Menck, Carlos F. M. |
author2_role |
author author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade de São Paulo (USP) Univ Paris Sud Universidade Federal de São Paulo (UNIFESP) Univ Fed Rio Grande do Sul Fed Univ Hlth Sci Porto Alegre UFCSPA |
dc.contributor.author.fl_str_mv |
Moraes, Maria Carolina S. Andrade, Annabel Quinet de Carvalho, Helotonio [UNIFESP] Guecheva, Temenouga Agnoletto, Mateus H. Henriques, Joao A. P. Sarasin, Alain Stary, Anne Saffi, Jenifer Menck, Carlos F. M. |
dc.subject.eng.fl_str_mv |
Doxorubicin DNA polymerase eta (pol eta) XPV XPA LY294002 DNA repair |
topic |
Doxorubicin DNA polymerase eta (pol eta) XPV XPA LY294002 DNA repair |
description |
Doxorubicin (DOX) is an important tumor chemotherapeutic agent, acting mainly by genotoxic action. This work focus on cell processes that help cell survival, after DOX-induced DNA damage. in fact, cells deficient for XPA or DNA polymerase eta (pol eta, XPV) proteins (involved in distinct DNA repair pathways) are highly DOX-sensitive. Moreover, LY294002, an inhibitor of PIKK kinases, showed a synergistic killing effect in cells deficient in these proteins, with a strong induction of G2/M cell cycle arrest. Taken together, these results indicate that XPA and pol eta proteins participate in cell resistance to DOX-treatment, and kinase inhibitors can selectively enhance its killing effects, probably reducing the cell ability to recover from breaks induced in DNA. (C) 2011 Elsevier Ireland Ltd. All rights reserved. |
publishDate |
2012 |
dc.date.issued.fl_str_mv |
2012-01-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:17:35Z |
dc.date.available.fl_str_mv |
2016-01-24T14:17:35Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Cancer Letters. Clare: Elsevier B.V., v. 314, n. 1, p. 108-118, 2012. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/34339 http://dx.doi.org/10.1016/j.canlet.2011.09.019 |
dc.identifier.issn.none.fl_str_mv |
0304-3835 |
dc.identifier.file.none.fl_str_mv |
WOS000298531900012.pdf |
dc.identifier.doi.none.fl_str_mv |
10.1016/j.canlet.2011.09.019 |
dc.identifier.wos.none.fl_str_mv |
WOS:000298531900012 |
identifier_str_mv |
Cancer Letters. Clare: Elsevier B.V., v. 314, n. 1, p. 108-118, 2012. 0304-3835 WOS000298531900012.pdf 10.1016/j.canlet.2011.09.019 WOS:000298531900012 |
url |
http://repositorio.unifesp.br/handle/11600/34339 http://dx.doi.org/10.1016/j.canlet.2011.09.019 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
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Cancer Letters |
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http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy info:eu-repo/semantics/openAccess |
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http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy |
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openAccess |
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108-118 |
dc.publisher.none.fl_str_mv |
Elsevier B.V. |
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Elsevier B.V. |
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