Publication:
Mitoxantrone potentiates TRAIL-induced apoptosis in glioblastoma multiforme

dc.contributor.coauthorAyhan, Ceyda Açılan
dc.contributor.departmentDepartment of Molecular Biology and Genetics
dc.contributor.departmentGraduate School of Health Sciences
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorCingöz, Ahmet
dc.contributor.kuauthorKaya, Ezgi
dc.contributor.kuauthorKazancıoğlu, Selena
dc.contributor.kuauthorLack, Nathan Alan
dc.contributor.kuauthorÖnder, Tuğba Bağcı
dc.contributor.kuauthorŞenbabaoğlu, Filiz
dc.contributor.schoolcollegeinstituteCollege of Sciences
dc.contributor.schoolcollegeinstituteGRADUATE SCHOOL OF HEALTH SCIENCES
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2024-11-09T23:50:55Z
dc.date.issued2016
dc.description.abstractGlioblastoma multiforme (GBM) is the most aggressive and frequent type of primary brain tumor with dismal survival rates. As GBM cells suppress apoptosis and evade death, re-activating dormant apoptotic programs with pro-apoptotic ligands or small molecules might be a promising approach. As such, the tumor-selective killing capacity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential treatment option in GBM. However, many tumor cells are intrinsically resistant and/or acquire resistance to TRAIL. In this study, we conducted an extensive drug-re-profiling screen to identify FDA-approved compounds that can be used clinically as TRAIL-sensitizing agents in GBM. Using selected isogenic GBM cell pairs with differential levels of TRAIL sensitivity, we revealed 26 TRAIL-sensitizing compounds, 13 of which were effective as single agents. One drug, Mitoxantrone, a DNA-damaging agent, did not cause toxicity to non-malignant cells at the doses that synergized with TRAIL on tumor cells. We investigated the downstream changes in apoptosis pathway components upon Mitoxantrone treatment, and observed that Death Receptors (DR4 and DR5) expression was upregulated, and pro-apoptotic and anti-apoptotic gene expression patterns were altered in favor of apoptosis. Together, our results suggest that combination of Mitoxantrone and TRAIL can be a promising therapeutic approach for GBM patients.
dc.description.indexedbyWOS
dc.description.openaccessNO
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.volume18
dc.identifier.doi10.1093/neuonc/now212.195
dc.identifier.eissn1523-5866
dc.identifier.issn1522-8517
dc.identifier.quartileQ1
dc.identifier.urihttps://doi.org/10.1093/neuonc/now212.195
dc.identifier.urihttps://hdl.handle.net/20.500.14288/14624
dc.keywordsOncology
dc.keywordsClinical neurology
dc.language.isoeng
dc.publisherOxford Univ Press
dc.relation.ispartofNeuro-Oncology
dc.subjectOncology
dc.subjectClinical neuropsychology
dc.titleMitoxantrone potentiates TRAIL-induced apoptosis in glioblastoma multiforme
dc.typeMeeting Abstract
dspace.entity.typePublication
local.contributor.kuauthorŞenbabaoğlu, Filiz
local.contributor.kuauthorCingöz, Ahmet
local.contributor.kuauthorKaya, Ezgi
local.contributor.kuauthorKazancıoğlu, Selena
local.contributor.kuauthorLack, Nathan Alan
local.contributor.kuauthorÖnder, Tuğba Bağcı
local.publication.orgunit1GRADUATE SCHOOL OF HEALTH SCIENCES
local.publication.orgunit1College of Sciences
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit2Department of Molecular Biology and Genetics
local.publication.orgunit2School of Medicine
local.publication.orgunit2Graduate School of Health Sciences
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