Glycogen synthase kinase-3 inhibition in glioblastoma multiforme cells induces apoptosis, cell cycle arrest and changing biomolecular structure

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dc.contributor.authorAcikgoz, Eda
dc.contributor.authorGuler, Gunnur
dc.contributor.authorCamlar, Mahmut
dc.contributor.authorOktem, Gulperi
dc.contributor.authorAktug, Huseyin
dc.date.accessioned2019-10-27T09:46:15Z
dc.date.available2019-10-27T09:46:15Z
dc.date.issued2019
dc.departmentEge Üniversitesien_US
dc.description.abstractGlioblastoma multiforme (GBM) is the most malignant and aggressive primary human brain tumors. The regulatory pathways of apoptosis are altered in GBMs, leading to a survival advantage of the tumor cells. Thus, identification of target molecules, which are effective in triggering of the cell death mechanisms in GBM, is an essential strategy for therapeutic purposes. Glycogen synthase kinase-3 (GSK-3) plays an important role in apoptosis, proliferation and cell cycle. This study focused on the effect of GSK-3 inhibitor IX in the GBM cells. Apoptosis induction was determined by Annexin-V assay, multicaspase activity and immunofluorescence analyses. Concentration-dependent effects of GSK-3 inhibitor IX on the cell cycle were also evaluated. Moreover, the effect of GSK inhibitor on the cellular biomolecules was assessed by using ATR-FTIR spectroscopy. Our assay results indicated that GSK-3 inhibitor IX induces apoptosis, resulting in a significant increase in the expression of caspase-3 and caspase-8 proteins. Cell cycle analyses revealed that GSK-3 inhibitor IX leads to dose -dependent G2/M-phase cell cycle arrest. Based on the FTIR data, treatment of GBM cells causes dysregulation in the carbohydrate metabolism and induces apoptotic cell death which was characterized by the spectral alterations in nucleic acids, an increment in the lipid amount with disordering state and compositional changes in the cellular proteins. These findings suggest that GSK-3 inhibitor IX exhibits anti-cancer effects by inducing apoptosis and changing biomolecular structure of membrane lipids, carbohydrates, nucleic acids and proteins, and thus, may be further evaluated as a potential effective candidate agent for the GBM combination therapies. (C) 2018 Elsevier B.V. All rights reserved.en_US
dc.identifier.doi10.1016/j.saa.2018.10.036en_US
dc.identifier.endpage164en_US
dc.identifier.issn1386-1425
dc.identifier.pmid30388586en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage150en_US
dc.identifier.urihttps://doi.org/10.1016/j.saa.2018.10.036
dc.identifier.urihttps://hdl.handle.net/11454/29250
dc.identifier.volume209en_US
dc.identifier.wosWOS:000453111700019en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherPergamon-Elsevier Science Ltden_US
dc.relation.ispartofSpectrochimica Acta Part A-Molecular and Biomolecular Spectroscopyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectGlioblastoma multiformeen_US
dc.subjectGlycogen synthase kinase-3en_US
dc.subjectApoptosisen_US
dc.subjectCell cycleen_US
dc.subjectATR-FTIR spectroscopyen_US
dc.subjectDrug action mechanismen_US
dc.titleGlycogen synthase kinase-3 inhibition in glioblastoma multiforme cells induces apoptosis, cell cycle arrest and changing biomolecular structureen_US
dc.typeArticleen_US

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