Gasimli, RoyaKayabasi, CaglaYelken, Besra OzmenAsik, AycanSogutlu, FatmaCelebi, CaglarSusluer, Sunde Yilmaz2024-08-252024-08-2520230955-30021362-3095https://doi.org/10.1080/09553002.2023.2232019https://hdl.handle.net/11454/100835PurposePI3K/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.en10.1080/09553002.2023.2232019info:eu-repo/semantics/closedAccessBreast cancerradiosensitivityPI3KmTOR pathwayPKI-402>Pi3k/Akt/Mtor Signaling PathwayCancer Stem-Cells3-Kinase/Mammalian TargetRadiationPhosphorylationRadioresistanceSurvivalAkt/PkbGsk-3Pi3kArticleWOS:0010267791000012-s2.0-8516513081137389464Q2Q1