ARID1A regulates cell proliferation through AKT signaling pathway in lung adenocarcinoma
10.16753/j.cnki.1008-2344.2025.03.004
- VernacularTitle:ARID1A通过AKT信号通路调控肺腺癌细胞增殖能力
- Author:
Zhirong LIU
1
;
Shufang ZHAO
;
Longfei WANG
Author Information
1. 蚌埠医科大学第一附属医院分子诊断中心,安徽 蚌埠 233000
- Publication Type:Journal Article
- Keywords:
ARID1A;
lung adenocarcinoma;
AKT;
cell proliferation
- From:
Journal of Shenyang Medical College
2025;27(3):244-249
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the regulatory role of the tumor suppressor gene ARID1A(AT-rich interaction domain 1A)in the proliferation of lung adenocarcinoma(LUAD)cells and its molecular mechanism associated with the protein kinase B(AKT)signaling pathway.Methods:Stable ARID1A-overexpressing A549/H1299 cell models were constructed via lentiviral transfection,with transfection efficiency validated by RT-PCR and Western blot.Cell viability was assessed using the CCK-8 assay,proliferation rate was evaluated using EdU staining,and migration capacity was analyzed by scratch assay.Cell death was evaluated through Calcein/PI live/dead staining and trypan blue exclusion.The phosphorylation level of AKT(p-AKT/AKT ratio)was detected by Western blot.The role of AKT in proliferation regulation was further validated by treating overexpressing cells with the AKT inhibitor MK-2206(1 μmol/L).Results:ARID1A overexpression significantly inhibited the proliferation and migration of A549/H1299 cells while upregulating p-AKT levels.MK-2206 treatment abolished the inhibitory effects of ARID1A overexpression on proliferation.Cell death assays demonstrated no significant impact of ARID1A overexpression on LUAD cell mortality.Conclusion:ARID1A specifically suppresses LUAD cell proliferation and migration by activating the AKT signaling pathway,suggesting that targeting AKT may provide a potential therapeutic strategy for LUAD patients with ARID1A deficiency.
