Inhibition of cell proliferation and migration by oxidative stress from ascorbate-driven juglone redox cycling in human bladder-derived T24 cells

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dc.contributor.authorKviecinski, M. R.
dc.contributor.authorPedrosa, R. C.
dc.contributor.authorFelipe, K. B.
dc.contributor.authorFarias, M. S.
dc.contributor.authorGlorieux, C.
dc.contributor.authorValenzuela, M.
dc.contributor.authorSid, B.
dc.contributor.authorBenites, J.
dc.contributor.authorValderrama, J. A.
dc.contributor.authorVerrax, J.
dc.contributor.authorBuc Calderon, P.
dc.date.accessioned2024-01-10T13:13:54Z
dc.date.available2024-01-10T13:13:54Z
dc.date.issued2012
dc.description.abstractThe effects of juglone on T24 cells were assessed in the presence and absence of ascorbate. The EC50 value for juglone at 24 h decreased from 28.5 mu M to 6.3 mu M in the presence of ascorbate. In juglone-treated cells, ascorbate increased ROS formation (4-fold) and depleted GSH (65%). N-acetylcysteine or catalase restricted the juglone/ascorbate-mediated effects, highlighting the role of oxidative stress in juglone cytotoxicity. Juglone alone or associated with ascorbate did not cause caspase-3 activation or PARP cleavage, suggesting necrosis-like cell death. DNA damage and the mild ER stress caused by juglone were both enhanced by ascorbate. In cells treated with juglone (1-5 mu M), a concentration-dependent decrease in cell proliferation was observed. Ascorbate did not impair cell proliferation but its association with juglone led to a clonogenic death state. The motility of ascorbate-treated cells was not affected. Juglone slightly restricted motility, but cells lost their ability to migrate most noticeably when treated with juglone plus ascorbate. We postulate that juglone kills cells by a necrosis-like mechanism inhibiting cell proliferation and the motility of T24 cells. These effects are enhanced in the presence of ascorbate. (C) 2012 Elsevier Inc. All rights reserved.
dc.description.funderBelgian Fonds National de la Recherche Scientifique (FNRS)
dc.description.funderNational Council for Scientific and Technological Development (CNPq) from Brazil
dc.description.funderFondo Nacional de Ciencia y Tecnologia from Chile
dc.fechaingreso.objetodigital20-03-2024
dc.format.extent6 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.bbrc.2012.03.150
dc.identifier.eissn1090-2104
dc.identifier.issn0006-291X
dc.identifier.pubmedidMEDLINE:22507983
dc.identifier.urihttps://doi.org/10.1016/j.bbrc.2012.03.150
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/78352
dc.identifier.wosidWOS:000304220200019
dc.information.autorucQuímica;Valderrama J;S/I;98772
dc.issue.numero2
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final273
dc.pagina.inicio268
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.revistaBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
dc.rightsacceso restringido
dc.subjectAscorbate
dc.subjectCell migration
dc.subjectJuglone
dc.subjectProliferation
dc.subjectRedox impairment
dc.subjectT24 cells
dc.subject1,4-NAPHTHOQUINONE
dc.subjectNAPHTHOQUINONES
dc.subjectANTHRACYCLINES
dc.subjectMECHANISM
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleInhibition of cell proliferation and migration by oxidative stress from ascorbate-driven juglone redox cycling in human bladder-derived T24 cells
dc.typeartículo
dc.volumen421
sipa.codpersvinculados98772
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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