Cell cycle kinetics, apoptosis rates, DNA damage and TP53 gene expression in bladder cancer cells treated with allyl isothiocyanate (mustard essential oil)

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dc.contributor.authorVentura Savio, Andre Luiz [UNESP]
dc.contributor.authorSilva, Glenda Nicioli da
dc.contributor.authorCamargo, Elaine Aparecida de [UNESP]
dc.contributor.authorSalvadori, Daisy Maria Favero [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de Ouro Preto (UFOP)
dc.date.accessioned2014-12-03T13:10:35Z
dc.date.available2014-12-03T13:10:35Z
dc.date.issued2014-04-01
dc.description.abstractAllyl isothiocyanate (AITC) is present in plants of the cruciferous family and is abundant in mustard seed. Due to its high bioavailability in urine after ingestion, AITC has been considered a promising antineoplastic agent against bladder cancer. Because TP53 mutations are the most common alterations in bladder cancer cells and are frequently detected in in situ carcinomas, in this study, we investigated whether the AITC effects in bladder cancer cells are dependent on the TP53 status. Two bladder transitional carcinoma cell lines were used: RT4, with wild-type TP53; and T24, mutated TP53 gene. AITC was tested at concentrations of 0.005, 0.0625, 0.0725, 0.0825, 0.0925, 0.125 and 0.25 mu M in cytotoxicity, cell and clonogenic survival assays, comet and micronucleus assays and for its effects on cell cycle and apoptosis by flow cytometry and on TP53 gene expression. The data showed increased primary DNA damage in both cell lines; however, lower concentrations of AITC were able to induce genotoxicity in the mutant cells for the TP53 gene. Furthermore, the results demonstrated increased apoptosis and necrosis rates in the wild-type cells, but not in mutated TP53 cells, and cell cycle arrest in the G2 phase for mutated cells after AITC treatment. No significant differences were detected in TP53 gene expression in the two cell lines. In conclusion, AITC caused cell cycle arrest, increased apoptosis rates and varying genotoxicity dependent on the TP53 status. However, we cannot rule out the possibility that those differences could reflect other intrinsic genetic alterations in the examined cell lines, which may also carry mutations in genes other than TP53. Therefore, further studies using other molecular targets need to be performed to better understand the mechanisms by which AITC may exert its antineoplastic properties against tumor cells. (C) 2014 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniv Estadual Paulista, Dept Patol, UNESP, Fac Med Botucatu, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationUFOP Univ Fed Ouro Preto, Escola Farm, Dept Anal Clin, BR-35400000 Ouro Preto, MG, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Patol, UNESP, Fac Med Botucatu, BR-18618970 Botucatu, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent40-46
dc.identifierhttp://dx.doi.org/10.1016/j.mrfmmm.2014.02.006
dc.identifier.citationMutation Research-fundamental And Molecular Mechanisms Of Mutagenesis. Amsterdam: Elsevier Science Bv, v. 762, p. 40-46, 2014.
dc.identifier.doi10.1016/j.mrfmmm.2014.02.006
dc.identifier.issn0027-5107
dc.identifier.lattes5051118752980903
dc.identifier.urihttp://hdl.handle.net/11449/112293
dc.identifier.wosWOS:000335105600006
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofMutation Research: Fundamental and Molecular Mechanisms of Mutagenesis
dc.relation.ispartofjcr2.398
dc.relation.ispartofsjr0,111
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectAllyl isothiocyanateen
dc.subjectApoptosisen
dc.subjectBladder canceren
dc.subjectCell cycleen
dc.subjectGenotoxicityen
dc.subjectTP53en
dc.titleCell cycle kinetics, apoptosis rates, DNA damage and TP53 gene expression in bladder cancer cells treated with allyl isothiocyanate (mustard essential oil)en
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
unesp.author.lattes5051118752980903
unesp.author.orcid0000-0001-9323-3134[4]
unesp.author.orcid0000-0001-6766-394X[1]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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