Antiproliferative effect of Potentilla fulgens on glioblastoma cancer cells through downregulation of Akt/mTOR signaling pathway

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dc.contributor.authorKandemir, Sevgi Irtegun
dc.contributor.authorIpek, Polat
dc.date.accessioned2024-04-24T17:24:15Z
dc.date.available2024-04-24T17:24:15Z
dc.date.issued2023
dc.departmentDicle Üniversitesien_US
dc.description.abstractBackground: Glioblastoma multiforme (GBM) is the most aggressive brain tumor that is common among adults. This aggression is due to increased invasion, migration, proliferation, angiogenesis, and decreased apoptosis. Plant-based compounds have a high potential to be used as an anticancer agent due to their various mechanisms and less undesirable side effects. Potentilla fulgens is a medicinal plant, and methanolic root extract of P. fulgens (PRE) has anti-inflammatory and anticancer properties.Objective: In this study, we aimed to investigate antiproliferative effect of PRE on U118 and T98G glioblastoma cancer cells and to reveal which molecular signaling pathways regulate this mechanism of action.Materials and Methods: The effect of PRE on cell viability of GBM cells was investigated by MTT assay. Involvement of PRE with cell growth and survival signaling pathways, phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR and c-Src/signal transducer and activator of transcription 3 (STAT3), was examined using Western Blot.Results: PRE reduced cell viability of GBM and human dermal fibroblast (HDF) cells in a dose-and time-independent manner. PI3K expression/phosphorylation level remained unchanged in both GBM and HDF cells after PRE treatment, but Akt/mTOR signaling pathway was downregulated in PRE-treated cells. PRE treatment did not affect c-Src expression/phosphorylation level in GBM cells; however, expression of c-Src was suppressed in HDF cells. Similar results were observed for STAT3 expression and phosphorylation status.Conclusion: PRE has the ability to suppress cell viability in GBM cells, by targeting the Akt/mTOR signaling pathway.en_US
dc.description.sponsorshipDicle University Scientific Research Projects Coordination Unit [DUBTAM.19.001]en_US
dc.description.sponsorshipThis study was supported by Dicle University Scientific Research Projects Coordination Unit with DUBTAM.19.001 project number.en_US
dc.identifier.doi10.4103/jcrt.jcrt_1886_21
dc.identifier.endpage1824en_US
dc.identifier.issn0973-1482
dc.identifier.issn1998-4138
dc.identifier.issue7en_US
dc.identifier.pmid38376284
dc.identifier.scopus2-s2.0-85170564186
dc.identifier.scopusqualityQ3
dc.identifier.startpage1818en_US
dc.identifier.urihttps://doi.org/10.4103/jcrt.jcrt_1886_21
dc.identifier.urihttps://hdl.handle.net/11468/19561
dc.identifier.volume19en_US
dc.identifier.wosWOS:001134479700035
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherWolters Kluwer Medknow Publicationsen_US
dc.relation.ispartofJournal of Cancer Research and Therapeutics
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAkt/Mtoren_US
dc.subjectGlioblastomaen_US
dc.subjectPotentilla Fulgensen_US
dc.subjectT98gen_US
dc.subjectU118en_US
dc.titleAntiproliferative effect of Potentilla fulgens on glioblastoma cancer cells through downregulation of Akt/mTOR signaling pathwayen_US
dc.titleAntiproliferative effect of Potentilla fulgens on glioblastoma cancer cells through downregulation of Akt/mTOR signaling pathway
dc.typeArticleen_US

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