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

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dc.contributor.author Moraes, Maria Carolina S.
dc.contributor.author Andrade, Annabel Quinet de
dc.contributor.author Carvalho, Helotonio [UNIFESP]
dc.contributor.author Guecheva, Temenouga
dc.contributor.author Agnoletto, Mateus H.
dc.contributor.author Henriques, Joao A. P.
dc.contributor.author Sarasin, Alain
dc.contributor.author Stary, Anne
dc.contributor.author Saffi, Jenifer
dc.contributor.author Menck, Carlos F. M.
dc.date.accessioned 2016-01-24T14:17:35Z
dc.date.available 2016-01-24T14:17:35Z
dc.date.issued 2012-01-01
dc.identifier http://dx.doi.org/10.1016/j.canlet.2011.09.019
dc.identifier.citation Cancer Letters. Clare: Elsevier B.V., v. 314, n. 1, p. 108-118, 2012.
dc.identifier.issn 0304-3835
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/34339
dc.description.abstract 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. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship USP-COFECUB (São Paulo, Brazil)
dc.format.extent 108-118
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Cancer Letters
dc.rights Acesso aberto
dc.subject Doxorubicin en
dc.subject DNA polymerase eta (pol eta) en
dc.subject XPV en
dc.subject XPA en
dc.subject LY294002 en
dc.subject DNA repair en
dc.title Both XPA and DNA polymerase eta are necessary for the repair of doxorubicin-induced DNA lesions en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Univ Paris Sud
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Univ Fed Rio Grande do Sul
dc.contributor.institution Fed Univ Hlth Sci Porto Alegre UFCSPA
dc.description.affiliation Univ São Paulo, Dept Microbiol, Inst Biomed Sci, São Paulo, Brazil
dc.description.affiliation Univ Paris Sud, Inst Gustave Roussy, Ctr Natl Rech Sci, UMR8200, Villejuif, France
dc.description.affiliation Fed Univ São Paulo UNIFESP, Dept Biol Sci, Diadema, SP, Brazil
dc.description.affiliation Univ Fed Rio Grande do Sul, Ctr Biotechnol, Dept Biophys, Porto Alegre, RS, Brazil
dc.description.affiliation Fed Univ Hlth Sci Porto Alegre UFCSPA, Dept Basic Hlth Sci, Porto Alegre, RS, Brazil
dc.description.affiliationUnifesp Fed Univ São Paulo UNIFESP, Dept Biol Sci, Diadema, SP, Brazil
dc.identifier.file WOS000298531900012.pdf
dc.identifier.doi 10.1016/j.canlet.2011.09.019
dc.description.source Web of Science
dc.identifier.wos WOS:000298531900012



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