Effects of α-hederin on proliferation,migration and apoptosis of 4T1 breast cancer cells via PI3K/Akt signaling pathway
10.3969/j.issn.1001-1528.2025.05.013
- VernacularTitle:α-常春藤皂苷通过调控PI3K/Akt信号通路对乳腺癌4T1细胞增殖、迁移和凋亡的影响
- Author:
Qian WANG
1
;
Chun-yu MA
1
Author Information
1. 锦州医科大学附属第一医院,辽宁锦州 121000
- Publication Type:Journal Article
- Keywords:
α-hederin;
breast cancer 4T1 cells;
PI3K/Akt signaling pathway;
proliferation;
migration;
apoptosis
- From:
Chinese Traditional Patent Medicine
2025;47(5):1502-1508
- CountryChina
- Language:Chinese
-
Abstract:
AIM To investigate the effects of α-hederin on proliferation,migration and apoptosis of 4T1 breast cancer cells.METHODS MTT assay was applied in the detection of proliferation of 4T1 cells treated with different concentrations of α-hederin(0,10,20,30,40,50,60 μmol/L).4T1 cells treated with different concentrations of α-hederin(0,10,20,30,40 μmol/L)had their morphologies observed;their ability of cell clone formation detected by clone formation experiment;their apoptosis detected by Hoechst 33342 staining;their apoptosis rate detected by Annexin V-FITC/PI double staining method;their cellular migration ability observed by cell scratch test;and their expressions of PI3K,p-PI3K,Akt,p-Akt,Bax,Bcl-2,cleaved Caspase3,cleaved PARP,E-cadherin,N-cadherin and Vimentin detected by Western blot.RESULTS Within the range of 10～60μmol/L α-hederin inhibited the proliferation of 4T1 cells in a concentration-dependent manner(P＜0.01),with an IC50 value of 29.8 μmoL/L within 24 h.Compared with the control(0 μmol/L)group,the groups intervened with 30 μmol/L or 40 μmnol/L α-hederin displayed significantly changed morphologies;decreased cellular clone-forming ability(P＜0.01);increased apopt otic cells counts(P＜0.01);increased apoptosis rate(P＜0.01);decreased cellular migration ability(P＜0.01);decreased p-PI3K,p-Akt,Bcl-2,N-cadherin and Vimentin protein expressions(P＜0.01);and increased protein expressions of Bax,cleaved Caspase3,cleaved PARP and E-cadherin(P＜0.01).CONCLUSION α-Hederin may induce the apoptosis of 4T1 cells through inhibiting their proliferation and migration via PI3K/Akt signaling pathway.
