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Bik subcellular localization in response to oxidative stress induced by chemotherapy, in Two different breast cancer cell lines and a Non-tumorigenic epithelial cell line

dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorAGLAE TREJO VARGASes_MX
dc.creatorELISA HERNANDEZ MERCADOes_MX
dc.creatorROSA MARIA ORDOÑEZ RAZOes_MX
dc.creatorROBERTO CARLOS LAZZARINI LECHUGAes_MX
dc.creatorDIEGO JULIO ARENAS ARANDAes_MX
dc.creatorMARIA CONCEPCION GUTIERREZ RUIZes_MX
dc.creatorMINA KONIGSBERG FAINSTEINes_MX
dc.creatorARMANDO LUNA LOPEZes_MX
dc.date2015
dc.date.accessioned2021-11-01T18:56:42Z
dc.date.available2021-11-01T18:56:42Z
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17303
dc.descriptionCancer chemotherapy remains one of the preferred therapeutic modalities against malignancies despite its damaging side effects. An expected outcome while utilizing chemotherapy is apoptosis induction. This is mainly regulated by a group of proteins known as the Bcl‐2 family, usually found within the endoplasmic reticulum or the mitochondria. Recently, these proteins have been located in other sites and non‐canonic functions have been unraveled. Bik is a pro‐apoptotic protein, which becomes deregulated in cancer, and as apoptosis is associated with oxidative stress generation, our objective was to determine the subcellular localization of Bik either after a direct oxidative insult due to H2O2, or indirectly by cisplatin, an antineoplastic agent. Experiments were performed in two human transformed mammary gland cell lines MDA‐MB‐231 and MCF‐7, and one non‐tumorigenic epithelial cell line MCF‐10A. Our results showed that in MCF‐7, Bik is localized within the cytosol and that after oxidative stress treatment it translocates into the nucleus. However, in MDA‐MB‐231, Bik localizes in the nucleus and translocates to the cytosol. In MCF10A Bik did not change its cellular site after either treatment. Interestingly, MCF10A were more resistant to cisplatin than transformed cell lines. This is the first report showing that Bik is located in different cellular compartments depending on the cancer stage, and it has the ability to change its subcellular localization in response to oxidative stress. This is associated with increased sensitivity when exposed to toxic agents, thus rendering novel opportunities to study new therapeutic targets allowing the development of more active and less harmful agents. Copyright © 2015 John Wiley & Sons, Ltd.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherWileyes_MX
dc.relationhttps://onlinelibrary.wiley.com/doi/abs/10.1002/jat.3173es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceJournal of Applied Toxicology (1099-1263) Vol. 35 (2015)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectQuímicaes_MX
dc.subjectBioqímicaes_MX
dc.subjectEstrés oxidativoes_MX
dc.subjectDrogas quimioterapéuticases_MX
dc.subjectOxidative stresses_MX
dc.subjectChemistryes_MX
dc.subjectBiochemistryes_MX
dc.subjectChemotherapeutic drugses_MX
dc.subjectCánceres_MX
dc.subjectCanceres_MX
dc.titleBik subcellular localization in response to oxidative stress induced by chemotherapy, in Two different breast cancer cell lines and a Non-tumorigenic epithelial cell linees_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
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dc.creator.nameIdentifiercurpes_MX
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