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Dakeun Lee,1 Eun Ji Yu,1 In-Hye Ham,2,3 Hoon Hur,2,3 You-Sun Kim4,5 1Department of Pathology, Ajou University School of Medicine, Suwon, Republic of Korea; 2Department of Surgery, Ajou University School of Medicine, Suwon, Republic of Korea; 3Brain Korea 21 Plus Research Center for Biomedical Sciences, Ajou University, Suwon, Republic of Korea; 4Department of Biochemistry, Ajou University School of Medicine, Suwon, Republic of Korea; 5Department of Biomedical Sciences, Graduate School, Ajou University, Suwon, Republic of Korea Background: The At-rich interactive domain 1A (ARID1A) is frequently mutated in gastric cancers (GCs) with a poor prognosis. Growing evidence indicates that loss of ARID1A expression leads to activation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway by AKT phosphorylation. We aim to investigate the different sensitivity for the AKT inhibitor in ARID1A-deficient GC cells. Methods: After transfection using siRNA or shRNA, the effect of ARID1A knockdown on the PI3K/AKT signaling pathway was evaluated by Western blot analysis. ARID1A-knockdown cells were treated with AKT inhibitor (GSK690693), 5-fluorouracil, or cisplatin, alone or in combination. Viability and apoptosis were analyzed using EZ-CYTOX cell viability assay and flow cytometry, respectively. Results: ARID1A depletion accelerated the phosphorylation of AKT and S6 in a dose-dependent manner and led to an increased proliferation of MKN-1, MKN-28, and KATO-III GC cells (P |
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