Punicic acid inhibits glioblastoma migration and proliferation via the PI3K/AKT1/mTOR signaling pathway

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dc.contributor.authorMete M.
dc.contributor.authorUnsal U.U.
dc.contributor.authorAydemir I.
dc.contributor.authorSönmez P.K.
dc.contributor.authorTuglu M.I.
dc.date.accessioned2024-07-22T08:09:02Z
dc.date.available2024-07-22T08:09:02Z
dc.date.issued2019
dc.description.abstractBackground: Punicic Acid (PA) is a polyunsaturated fatty acid that accounts for approximately 70%- 80% of Pomegranate Seed Oil (PSO). PA possesses strong antioxidant, anti-inflammatory, anti-atherogenic effects, and anti-tumorigenic properties. Pomegranate extracts have been shown to have anticancer activity in many studies. However, there is no evidence for the effect of PSO on T98 glioblastoma cells. Therefore, the present study was the first to investigate the mechanisms induced by PA on T98 cells, which is one of the major compounds extracted from PSO. Methods: The effects of PA on cell viability; oxidative stress; and migration, proliferation, and apoptosis at the IC50 dose were studied. Results: The proliferation and migration were inhibited in the treated group compared to the non-treated group by 9.85μl/ml PA. The difference was statistically significant (***p<0.001). Furthermore, PA-induced apoptosis in the T98 glioblastoma cells compared to non-treated group and the difference was statistically significant (***p<0.001). Apoptosis was determined via immunocytochemistry staining of caspase-3, caspase-9 and TUNEL methods. Apoptosis was checked by flow cytometry (using caspase 3 methods) and Scanning Electron Microscopy Analysis. We also investigated the potential signaling pathway underlying this apoptotic effect. The immunocytochemical stainings of PI3K/ Akt-1/ mTOR-1 demonstrated that Akt-1 staining was increased with PA treatment similar to mTOR-1 and PI3K staining (***p<0.001). These increases were statistically significant compared to the non-treated group. Conclusion: PA exhibited exceptional abilities as an anticancer agent against GBM cells. The use of punicic acid in combination with other drugs used in the treatment of glioblastoma may increase the efficacy of the treatment. This study provided a basis for future investigation of its use in preclinical and clinical studies. © 2019 Bentham Science Publishers.
dc.identifier.DOI-ID10.2174/1871520619666190405112507
dc.identifier.issn18715206
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/14644
dc.language.isoEnglish
dc.publisherBentham Science Publishers
dc.subjectCell Line, Tumor
dc.subjectCell Movement
dc.subjectCell Proliferation
dc.subjectCell Survival
dc.subjectDose-Response Relationship, Drug
dc.subjectDrug Screening Assays, Antitumor
dc.subjectGlioblastoma
dc.subjectHumans
dc.subjectLinolenic Acids
dc.subjectMolecular Structure
dc.subjectOxidative Stress
dc.subjectPhosphatidylinositol 3-Kinases
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectSignal Transduction
dc.subjectStructure-Activity Relationship
dc.subjectTOR Serine-Threonine Kinases
dc.subjectantineoplastic agent
dc.subjectcaspase 3
dc.subjectcaspase 9
dc.subjectendothelial nitric oxide synthase
dc.subjectinducible nitric oxide synthase
dc.subjectmammalian target of rapamycin complex 1
dc.subjectmatrix metalloproteinase 20
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectprotein p53
dc.subjectpunicic acid
dc.subjecttransforming growth factor beta1
dc.subjectunclassified drug
dc.subjectvasculotropin
dc.subjectAKT1 protein, human
dc.subjectlinolenic acid
dc.subjectMTOR protein, human
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectpunicic acid
dc.subjecttarget of rapamycin kinase
dc.subjectAkt signaling
dc.subjectangiogenesis
dc.subjectapoptosis
dc.subjectArticle
dc.subjectcancer inhibition
dc.subjectcell death
dc.subjectcell migration
dc.subjectcell proliferation
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectcytotoxicity
dc.subjectflow cytometry
dc.subjectfluorescence microscopy
dc.subjectglioblastoma
dc.subjecthuman
dc.subjecthuman cell
dc.subjectIC50
dc.subjectimmunocytochemistry
dc.subjectmetastasis
dc.subjectMTT assay
dc.subjectoxidative stress
dc.subjectscanning electron microscopy
dc.subjectT98 cell line
dc.subjectTUNEL assay
dc.subjectvascularization
dc.subjectWestern blotting
dc.subjectwound healing assay
dc.subjectcell motion
dc.subjectcell proliferation
dc.subjectcell survival
dc.subjectchemical structure
dc.subjectchemistry
dc.subjectdose response
dc.subjectdrug effect
dc.subjectdrug screening
dc.subjectglioblastoma
dc.subjectmetabolism
dc.subjectpathology
dc.subjectsignal transduction
dc.subjectstructure activity relation
dc.subjectsynthesis
dc.subjecttumor cell line
dc.titlePunicic acid inhibits glioblastoma migration and proliferation via the PI3K/AKT1/mTOR signaling pathway
dc.typeArticle

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