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Characterization of the NF-?B signaling triggered by doxorubicin.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lopez de Vergara, Oihana Pablos, Raquel Ruiz-Sanz, M. Begoña Ruiz-Larrea, José Ignacio Navarro, Rosaura
Description	Author Affiliation: Lopez de Vergara O ( University of Basque Country UPV/EHU (Faculty of Medicine and Dentistry), Department of Physiology, Spain.. Electronic address: oihanala@hotmail.com.); Pablos R ( University of Basque Country UPV/EHU (Faculty of Medicine and Dentistry), Department of Physiology, Spain.); Ruiz-Sanz MB ( University of Basque Country UPV/EHU (Faculty of Medicine and Dentistry), Department of Physiology, Spain.); Ruiz-Larrea JI ( University of Basque Country UPV/EHU (Faculty of Medicine and Dentistry), Department of Physiology, Spain.); Navarro R ( University of Basque Country UPV/EHU (Faculty of Medicine and Dentistry), Department of Physiology, Spain.)
Abstract	Doxorubicin (DOX) is an antibiotic used in the treatment of various cancers. However, its clinical use is limited due to the toxic effects it causes. In several biological systems reactive oxygen species (ROS) derived from DOX metabolism have been associated with its toxicity because they can alter several signal transduction pathways. One of the major signal transduction pathways activated in response to oxidant stress is that of the nuclear transcription factor ?B (NF-?B), which is crucial for cell survival, cell proliferation, and immune responses. Previous studies from our laboratory have described that DOX triggersthe activation of the MAPK (ERK, p38, and JNK) pathways, NF-?B mobilization and caspase activation in rat hepatocytes. These events were indirectly ascribed to ROS generation by pharmacological approaches. Although NF-?B mobilization is usually accompanied by up-regulation of the genes with regulatory ?B elements, our gene expression analysis rendered a quite different scenario. The aim of this work was to verify the implication of ROS in the DOX-mediated signaling and to explore the transcriptional regulatory behaviour of NF-?B mobilized by DOX. Results showed that DOX treatment induces ROS generation, particularly H2O2. DOX-induced caspase-3 activation was ROS dependent, whereas the NF-?B mobilization was a process independent of H2O2. Furthermore, DOX-mobilized NF-?B complexes were dimmers formed by p65 with all the members of the Rel family, excepting Rel B. The analysis of the NF-?B transcriptional activity performed by reporter gene assays suggests that these DOX-mobilized NF-?B complexes are not transcriptionally competent.
File Format	HTM / HTML
ISSN	08915849
Issue Number	Suppl 1
Journal	Free Radical Biology and Medicine
Volume Number	75
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2014-10-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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