Clostridium botulinum neurotoxin A inhibits DBTRG glioblastoma cell proliferation and TRPV1 channel signaling pathways

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dc.authorscopusid56033997900
dc.contributor.authorAkyuva, Yener
dc.date.accessioned2024-09-19T15:48:31Z
dc.date.available2024-09-19T15:48:31Z
dc.date.issued2020
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractPrevalence of glioblastomas is high within the adult brain tumors and the proliferation of the glioblastomas was induced by excessive Ca2+ influx. Ca2+ permeable TRPV1 channel is gated by capsaicin and reactive oxygen species (ROS), although its activity was decreased in neurons by AMG and antioxidants. Clostridium botulinum neurotoxin A (BotxA) acted antioxidant action in several cells and its treatment modulated TRPV1 in neurons. Hence, treatment of BotxA may modulate glioblastoma cell proliferation and death via inhibition of TRPV1 in the DBTRG glioblastoma in vitro cell line model. The DBTRG cells were divided into three groups as control, BotxA (5 IU for 24 hours) and BotxA+TRPV1 channel blocker (AMG and 1 µM for 30 min). Intracellular Ca2+ response to TRPV1 activation was increased in the cells from capsaicin, although it was reduced by the BotxA and AMG. BotxA treatment decreased cell proliferation, although its treatment increased cell death (propidium iodide/Hoechst rate). In addition, BotxA decreased mitochondrial membrane depolarization levels, cytosolic and mitochondrial ROS generation in the cells. Their levels were further decreased in the BotxA+AMG group by the AMG treatment. The antiproliferative and neurotoxic effects of BotxA were shown to be exerted via modulation of oxidative stress and TRPV1 activation. BotxA could be used as an effective agent in the treatment of glioblastoma proliferation. © 2020 Suleyman Demirel University. All rights reserved.en_US
dc.description.sponsorshipBSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture, Industry and Trade Limited Company, (2018-32)en_US
dc.identifier.doi10.37212/JCNOS.809635
dc.identifier.endpage913en_US
dc.identifier.issn2149-7222
dc.identifier.issue1en_US
dc.identifier.scopus2-s2.0-85096022421en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage903en_US
dc.identifier.urihttps://doi.org/10.37212/JCNOS.809635
dc.identifier.urihttps://hdl.handle.net/20.500.12483/15119
dc.identifier.volume12en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherSuleyman Demirel Universityen_US
dc.relation.ispartofJournal of Cellular Neuroscience and Oxidative Stressen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectGlioblastomaen_US
dc.subjectMitochondriaen_US
dc.subjectOxidative stressen_US
dc.subjectProliferationen_US
dc.subjectTRPV1 channelen_US
dc.titleClostridium botulinum neurotoxin A inhibits DBTRG glioblastoma cell proliferation and TRPV1 channel signaling pathwaysen_US
dc.typeArticleen_US

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