Demethylzeylasteral inhibits proliferation,migration and invasion and promotes apoptosis of non-small cell lung cancer cells by inhibiting the AKT/CREB signaling pathway
10.12122/j.issn.1673-4254.2024.02.10
- VernacularTitle:去甲泽拉木醛通过抑制AKT/CREB信号通路抑制非小细胞肺癌细胞的增殖、迁移和侵袭
- Author:
Qiqi HAN
1
;
Mengran YE
;
Qili JIN
Author Information
1. 蚌埠医科大学检验医学院,安徽 蚌埠 233030
- Keywords:
non-small cell lung cancer;
demethylzeylasteral;
AKT;
CREB
- From:
Journal of Southern Medical University
2024;44(2):280-288
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism underlying the inhibitory effects of Demethylzeylasteral(T-96)on non-small cell lung cancer(NSCLC)cells.Methods We first examined the effects of different concentrations(1,3,10,and 30 μmol/L)of demethylzeylasteral on morphology and cell number of A549 and H1299 cells.The changes in proliferation,cell viability,migration,invasion,and apoptosis of A549 and H1299 cells following demethylzeylasteral treatment were detected using clone formation,CCK-8,cell scratch,Transwell,and flow cytometric assays,and the effect of SC79 treatment against demethylzeylasteral-induced cell apoptosis was assessed.Western blotting was performed to detect the changes in expressions of E-cadherin,N-cadherin,vimentin,Bax,Bcl-2 and cleaved caspase-3 and phosphorylation of AKT/CREB in demethylzeylasteral-treated A549 and H1299 cells and the cellular expressions of apoptotic proteins following treatment with both demethylzeylasteral and SC79.Results T-96 treatment caused elongation of the cell body and widening of the intercellular space and significantly inhibited cell viability,proliferation,migration and invasion of A549 and H1299 cells(P<0.05).Flow cytometry showed that demethylzeylasteral induced apoptosis in both A549 and H1299 cells,whereas SC79 treatment obviously attenuated its pro-apoptotic effect(P<0.05).Western blotting revealed up-regulated expressions of Bax and cleaved caspase-3 proteins and lowered Bcl-2 expression level in demethylzeylasteral-treated A549 and H1299 cells,but co-treatment with SC79 obviously attenuated the expressions of the apoptotic proteins.T-96 significantly up-regulated the expression level of E-cadherin,down-regulated the expressions of N-cadherin and vimentin,and inhibited the phosphorylation of AKT and CREB in the two cell lines(P<0.05).Conclusion T-96 inhibits the proliferation,migration and invasion and induces apoptosis of NSCLC cells possibly by inhibiting the AKT/CREB signaling pathway.
