Publication:
Temozolomide increases heat shock proteins in extracellular vesicles released from glioblastoma cells

dc.contributor.coauthorKıyga, E.
dc.contributor.coauthorÖnay Uçar, E.
dc.contributor.kuauthorAdıgüzel, Zelal
dc.contributor.kuprofileFaculty Member
dc.contributor.schoolcollegeinstituteSchool of Medicine
dc.date.accessioned2024-11-09T11:55:14Z
dc.date.issued2022
dc.description.abstractBackground: Glioblastoma (GBM) is the most malignant and the fastest-progressing type of primary brain tumours. Temozolomide (TMZ) is a chemotherapeutic drug for the treatment of GBM. Extracellular vesicles (EVs) have been recently confirmed to have a substantial role in the GBM, and their contents released from GBM cells have been considered a target for treatment. The purpose of this study is to evaluate the impact of TMZ on heat shock proteins (HSPs) derived from EVs originated from GBM cell lines (U87-MG and LN229) and the significance of EVs in response to chemotherapy in GBM. Methods and results: NTA, ELISA, and immunoblotting were used to characterization studies of EVs and results showed that U87-MG cells released many EVs compared to LN229 cells. The effect of TMZ treatments on HSPs expression levels were assessed with immunoblotting and was found to be led to increases in HSF-1, Hsp90, Hsp70, Hsp60 and Hsp27 expression in GBM cells and their EV contents, which these increases are related to therapeutic resistance. What is more, in Real-time PCR studies showing which signalling pathways might be associated with these increases, it was observed that TMZ triggered the expression of RAD51 and MDM2 genes in cells and EV contents. More strikingly, we discover a correlation between EV and parental cells in regard of mRNA and protein level in both cell lines as a result of TMZ treatment. Conclusions: our data suggest of EVs in the treatment of GBM may have potential biomarkers that can be used to investigate the treatment response.
dc.description.fulltextYES
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue9
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuTÜBİTAK
dc.description.sponsorshipIstanbul University Scientifc Research Projects (BAP) Coordination Unit
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TÜBİTAK)
dc.description.versionAuthor's final manuscript
dc.description.volume49
dc.formatpdf
dc.identifier.doi10.1007/s11033-022-07714-5
dc.identifier.eissn1573-4978
dc.identifier.embargoNO
dc.identifier.filenameinventorynoIR03843
dc.identifier.issn0301-4851
dc.identifier.linkhttps://doi.org/10.1007/s11033-022-07714-5
dc.identifier.quartileQ3
dc.identifier.scopus2-s2.0-85132815879
dc.identifier.urihttps://hdl.handle.net/20.500.14288/819
dc.identifier.wos815562200003
dc.keywordsDrug resistance
dc.keywordsExtracellular vesicles
dc.keywordsGlioblastoma
dc.keywordsHSP
dc.keywordsTemozolomide
dc.languageEnglish
dc.publisherSpringer
dc.relation.grantno33460
dc.relation.grantno216S973
dc.relation.urihttp://cdm21054.contentdm.oclc.org/cdm/ref/collection/IR/id/10701
dc.sourceMolecular Biology Reports
dc.subjectMedicine
dc.titleTemozolomide increases heat shock proteins in extracellular vesicles released from glioblastoma cells
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorAdıgüzel, Zelal

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