Clostridium botulinumneurotoxin A induces apoptosis and mitochondrial oxidative stress via activation of TRPM2 channel signaling pathway in neuroblastoma and glioblastoma tumor cells

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dc.contributor.authorAkpınar, Orhan
dc.contributor.authorÖzşimşek, Ahmet
dc.contributor.authorGüzel, Mustafa
dc.contributor.authorNazıroğlu, Mustafa
dc.date.accessioned2021-02-19T21:16:33Z
dc.date.available2021-02-19T21:16:33Z
dc.date.issued2020
dc.departmentALKÜ
dc.description.abstractBackground TheClostridium botulinumneurotoxin A (BTX) is a polypeptide produced by the bacteriumClostridium botulinum. In addition to the therapeutic actions of BTX against pain and neuromuscular disorders, it is acted as anticancerogenic effect through excessive mitochondria reactive oxygen species (ROS) production, apoptosis, and caspase activations. The TRPM2 cation channel is activated by ROS and ADP-ribose and it is inhibited by 2-aminoethyl diphenylborinate (2-APB) and N-(p-amylcinnamoyl) anthranilic acid (ACA). The aim of this study was an investigation of involvement BTX-induced TRPM2 activation on the mitochondria ROS production and apoptosis levels in the DBTRG glioblastoma and SH-SY5Y neuroblastoma tumor cells. Material and methods The DBTRG and SH-SY5Y cells were divided into four groups as control, BTX (5 IU for 24 h), BTX + ACA (25 mu M for 30 min), and BTX + 2-APB (100 mu M for 30 min). Results BTX treatment increased mitochondrial membrane depolarization (JC-1), mitochondrial (MitROS), and cytosolic (DHR123 and DCFH-DA) ROS levels, neuronal death (propidium iodide/Hoechst) rate, caspase -3, and -9 levels in the BTX group, although their levels were diminished in the BTX + ACA and BTX + 2-APB groups. The ACA and 2-APB treatments also decreased BTX-induced increase of TRPM2 cytosolic free Ca(2+)concentration in the glioblastoma and neuroblastoma cell death. Conclusions BTX caused neuroblastoma and glioblastoma tumor cell death by activating the mitochondria ROS productionviastimulating TRPM2 signaling pathways. BTX may serve as a potential therapeutic targetviaactivation of TRPM2 for treating glioblastoma and neuroblastoma cells.
dc.description.sponsorshipBSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture, Industry and Trade Limited Company, Goller Bolgesi Teknokenti, Isparta, Turkey [2018-21]
dc.description.sponsorshipThe study was supported by BSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture, Industry and Trade Limited Company, Goller Bolgesi Teknokenti, Isparta, Turkey (Project No: 2018-21).
dc.identifier.doi10.1080/10799893.2020.1781174
dc.identifier.endpage632en_US
dc.identifier.issn1079-9893
dc.identifier.issn1532-4281
dc.identifier.issue6en_US
dc.identifier.pmid32646271
dc.identifier.scopusqualityQ2
dc.identifier.startpage620en_US
dc.identifier.urihttps://doi.org/10.1080/10799893.2020.1781174
dc.identifier.urihttps://hdl.handle.net/20.500.12868/471
dc.identifier.volume40en_US
dc.identifier.wosWOS:000547061400001
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthor0-belirlenecek
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofJournal of Receptors And Signal Transduction
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectApoptosis
dc.subjectClostridium botulinumneurotoxin A
dc.subjectglioblastoma death
dc.subjectmitochondria oxidative stress
dc.subjectTRPM2 channel
dc.titleClostridium botulinumneurotoxin A induces apoptosis and mitochondrial oxidative stress via activation of TRPM2 channel signaling pathway in neuroblastoma and glioblastoma tumor cells
dc.typeArticle

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