Publication:
Nrf2 silencing to inhibit proteolytic defense induced by hyperthermia in HT22 cells

dc.contributor.authorYILMAZ, BETÜL
dc.contributor.authorsBozaykut, Perinur; Ozer, Nesrin Kartal; Karademir, Betul
dc.date.accessioned2022-03-14T08:14:47Z
dc.date.available2022-03-14T08:14:47Z
dc.date.issued2016-08
dc.description.abstractNrf2 pathway has been known to be protective against cancer progression however recent studies have revealed that the antioxidant activity of Nrf2 contributes to chemotherapy resistance. For many years, hyperthermia has been used as an additional therapy to increase the efficiency of chemotherapy and radiotherapy. Besides the positive effects of hyperthermia during treatment procedure, thermotolerance has been found to develop against heat treatment. Although the involved molecular mechanisms have not been fully clarified, heat shock proteins (HSP) and proteasome activity are known to be involved in the acquisition of thermotolerance. The aim of this study was to investigate the potential beneficial effects of combining hyperthermia with Nrf2 silencing to inhibit molecular mechanisms leading to induction of defense mechanisms in transcription level. Following heat treatment of HT22 cells, HSP70 and the proteasome levels and as well as proteasome activity were found to be elevated in the nucleus. Our results demonstrated that Nrf2 silencing reduced defense mechanisms against heat treatment both in antioxidant and proteolytic manner and Nrf2 may be a potential target for therapeutic approach in order to improve the beneficial effects of hyperthermia in cancer therapy. (C) 2016 The Authors. Published by Elsevier B.V.
dc.identifier.doi10.1016/j.redox.2016.03.001
dc.identifier.issn2213-2317
dc.identifier.pubmed26966891
dc.identifier.urihttps://hdl.handle.net/11424/241279
dc.identifier.wosWOS:000377427000035
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofREDOX BIOLOGY
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNrf2
dc.subjectHyperthermia
dc.subjectProteasome
dc.subjectHeat shock proteins
dc.subjectHEAT-SHOCK PROTEINS
dc.subjectUBIQUITIN-PROTEASOME PATHWAY
dc.subjectOXIDATIVE STRESS
dc.subjectBREAST-CANCER
dc.subjectCARCINOMA-CELLS
dc.subjectHELA-CELLS
dc.subjectINDUCTION
dc.subjectAPOPTOSIS
dc.subjectACTIVATION
dc.subjectHSP90
dc.titleNrf2 silencing to inhibit proteolytic defense induced by hyperthermia in HT22 cells
dc.typearticle
dspace.entity.typePublication
local.avesis.id9cc22782-15e5-4643-91e7-e4eb4938dc29
local.import.packageSS16
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages10
local.journal.quartileQ1
oaire.citation.endPage332
oaire.citation.startPage323
oaire.citation.titleREDOX BIOLOGY
oaire.citation.volume8
relation.isAuthorOfPublication81633a07-e5fb-4760-b3ef-bf0878d87827
relation.isAuthorOfPublication.latestForDiscovery81633a07-e5fb-4760-b3ef-bf0878d87827

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