The effects of PKI-402 on breast tumor models' radiosensitivity via dual inhibition of PI3K/mTOR

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dc.authoridASIK, AYCAN/0000-0002-4123-4175
dc.authoridGASIMLI, Roya/0000-0002-6760-8921
dc.authoridSogutlu, Fatma/0000-0002-1210-7660
dc.authorscopusid57203593277
dc.authorscopusid56497855800
dc.authorscopusid57191416192
dc.authorscopusid56441719900
dc.authorscopusid57203588534
dc.authorscopusid57216455346
dc.authorscopusid54889084200
dc.authorwosidASIK, AYCAN/A-8211-2019
dc.contributor.authorGasimli, Roya
dc.contributor.authorKayabasi, Cagla
dc.contributor.authorYelken, Besra Ozmen
dc.contributor.authorAsik, Aycan
dc.contributor.authorSogutlu, Fatma
dc.contributor.authorCelebi, Caglar
dc.contributor.authorSusluer, Sunde Yilmaz
dc.date.accessioned2024-08-25T18:37:04Z
dc.date.available2024-08-25T18:37:04Z
dc.date.issued2023
dc.departmentEge Üniversitesien_US
dc.description.abstractPurposePI3K/Akt/mTOR pathway activation causes relapse and resistance after radiotherapy in breast cancer (BC). We aimed to radiosensitize BC cell lines to irradiation (IR) by PKI-402, a dual PI3K/mTOR inhibitor.MethodsWe performed cytotoxicity, clonogenicity, hanging drop, apoptosis and double-strand break detection, and phosphorylation of 16 essential proteins involved in the PI3K/mTOR pathway.ResultsOur findings showed that PKI-402 has cytotoxic efficiency in all cell lines. Clonogenic assay results showed that PKI-402 plus IR inhibited the colony formation ability of MCF-7 and breast cancer stem cell lines. Results showed that PKI-402 plus IR causes more apoptotic cell death than IR alone in the MCF-7 cells but did not cause significant changes in the MDA-MB-231. & gamma;-H2AX levels were increased in MDA-MB-231 in PKI-402 plus IR groups, whereas we did not observe any apoptotic and & gamma;-H2AX induction in BCSCs and MCF-10A cells in all treatment groups. Some pivotal phosphorylated proteins of the PI3K/AKT pathway decreased, several proteins increased and others did not change.ConclusionIn conclusion, if the combined use of PKI-402 with radiation is supported by in vivo studies, it can contribute to the treatment options and the course of the disease.en_US
dc.description.sponsorshipEge University Scientific Research Projects (BAP) Department [2017-TIP-022, 18-KSUAM-001]en_US
dc.description.sponsorshipThis study was supported by Ege University Scientific Research Projects (BAP) Department (Grant No. 2017-TIP-022, 18-KSUAM-001).en_US
dc.identifier.doi10.1080/09553002.2023.2232019
dc.identifier.issn0955-3002
dc.identifier.issn1362-3095
dc.identifier.pmid37389464en_US
dc.identifier.scopus2-s2.0-85165130811en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1080/09553002.2023.2232019
dc.identifier.urihttps://hdl.handle.net/11454/100835
dc.identifier.wosWOS:001026779100001en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofInternational Journal of Radiation Biologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz20240825_Gen_US
dc.subjectBreast canceren_US
dc.subjectradiosensitivityen_US
dc.subjectPI3Ken_US
dc.subjectmTOR pathwayen_US
dc.subjectPKI-402en_US
dc.subject>en_US
dc.subjectPi3k/Akt/Mtor Signaling Pathwayen_US
dc.subjectCancer Stem-Cellsen_US
dc.subject3-Kinase/Mammalian Targeten_US
dc.subjectRadiationen_US
dc.subjectPhosphorylationen_US
dc.subjectRadioresistanceen_US
dc.subjectSurvivalen_US
dc.subjectAkt/Pkben_US
dc.subjectGsk-3en_US
dc.subjectPi3ken_US
dc.titleThe effects of PKI-402 on breast tumor models' radiosensitivity via dual inhibition of PI3K/mTORen_US
dc.typeArticleen_US

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