Chromosomal aberrations induced by 5-azacytidine combined with VP-16 (etoposide) in CHO-K1 and XRS-5 cell lines

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorGuimaraes, APA
dc.creatorDias, F. L.
dc.creatorCardoso, R. S.
dc.creatorKronka, S. N.
dc.creatorSakamoto-Hojo, E. T.
dc.date2014-05-20T13:13:29Z
dc.date2016-10-25T16:34:15Z
dc.date2014-05-20T13:13:29Z
dc.date2016-10-25T16:34:15Z
dc.date2003-01-01
dc.date.accessioned2017-04-05T19:21:59Z
dc.date.available2017-04-05T19:21:59Z
dc.identifierTeratogenesis Carcinogenesis and Mutagenesis. New York: Wiley-liss, p. 171-186, 2003.
dc.identifier0270-3211
dc.identifierhttp://hdl.handle.net/11449/1255
dc.identifierhttp://acervodigital.unesp.br/handle/11449/1255
dc.identifier10.1002/tcm.10072
dc.identifierWOS:000181335300016
dc.identifierhttp://dx.doi.org/10.1002/tcm.10072
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/851318
dc.descriptionA cytogenetic study was carried out with 5-azacytidine (5-azaC) and etoposide (VP-16) in CHO-K1 and XRS-5 (mutant cells deficient for double-strand break rejoining) cell lines to verify the interaction effects of the drugs in terms of induction of chromosomal aberrations. 5-azaC is incorporated into DNA causing DNA hypomethylation, and VP-16 (inhibitor of topoisomerase 11 enzyme) is a potent clastogenic agent. Cells in exponential growth were treated with 5-azaC for I h, following incubation for 7 h, and posttreatment with VP16 for the last 3 h. In K1 cells, the combined treatments induced a significant reduction in the aberrations induced in the X and A (autosome) chromosomes, which are the main target for 5-azaC. However, in XRS-5 cells, the drug combination caused a significant increase in the aberrations induced in those chromosomes, but with a concomitant reduction in the randomly induced-aberrations. In addition, each cell line presented characteristic cell cycle kinetics; while the combined treatment induced an S-arrest in K1 cells, alterations in cell cycle progression were not found for XRS-5, although each drug alone caused a G2-arrest. The different cell responses presented by the cell lines may be explained on the basis of the evidence that alterations in chromatin structure caused by 5-aza-C probably occur to a different extent in K1 and XRS-5 cells, since the mutant cells present a typical hyper-condensed chromosome structure (especially the X- and A chromosomes), but, alternatively, 5-aza-C could induce reactivation of DNA repair genes in XRS-5 cells. Teratogenesis Carcinog. Mutagen. Suppl. 1:171-186, 2003. (C) 2003 Wiley-Liss, Inc.
dc.languageeng
dc.publisherWiley-Blackwell
dc.relationTeratogenesis Carcinogenesis and Mutagenesis
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subject5-azacytidine
dc.subjectetoposide
dc.subjectchromosomal aberrations
dc.subjectDNA methylation
dc.titleChromosomal aberrations induced by 5-azacytidine combined with VP-16 (etoposide) in CHO-K1 and XRS-5 cell lines
dc.typeOtro


Este ítem pertenece a la siguiente institución