Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions

Detalhes bibliográficos
Autor(a) principal: Moraes, Maria Carolina S.
Data de Publicação: 2012
Outros Autores: 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.
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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spelling 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
dc.relation.ispartof.none.fl_str_mv Cancer Letters
dc.rights.driver.fl_str_mv http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 108-118
dc.publisher.none.fl_str_mv Elsevier B.V.
publisher.none.fl_str_mv Elsevier B.V.
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
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institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
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