Digoxin and Tamoxifen synergistically suppress proliferation, migration and invasion in breast cancer MCF-7 cells
10.3969/j.issn.1001-1978.2021.09.013
- Author:
Jing-Kun SHEN
1
;
Jia-Bin MEI
1
;
Ji-Gang PAN
1
;
Lu WANG
1
;
Xu-Dong WANG
1
;
Hai-Tao ZHU
2
Author Information
1. Dept of Physiology, School of Basic Medicine, Guizhou Medical University
2. Dept of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University
- Publication Type:Journal Article
- Keywords:
breast cancer cells;
digoxin;
epithelial-mesenchy-mal transition;
proliferation;
synergistic action;
tamoxifen
- From:
Chinese Pharmacological Bulletin
2021;37(9):1256-1263
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of digoxin combined with tamoxifen on proliferation, migration, invasion of breast cancer MCF-7 cells and the possible underlying mechanism. Methods MTT, colony formation and flow cytometry were used to detect the effect of the combination therapy of tamoxifen and digoxin on proliferation and apoptosis in MCF-7 cells. Wound healing assay and transwell assay were used to detect the effect of the combination therapy of tamoxifen and digoxin on migration and invasion of MCF-7 cells. Western blot was used to detect the effect of the combination therapy of tamoxifen and digoxin on the expression of related proteins in MCF-7 cells. Results MTT, colony formation assay and flow cytometry results showed that digoxin and tamoxifen synergistically inhibited the proliferation and promoted the apoptosis of MCF-7 cells. Wound healing and transwell assay results showed that digoxin and tamoxifen synergistically inhibited the migration and invasion of MCF-7 cells. Western blot results showed that digoxin and tamoxifen synergistically inhibited the expression of PI3K, p-PI3K, p-AKT, Bcl-2, N-cadherin, Vimentin and promoted the expression of Bax, cleaved-caspase-3, cleaved-caspase-9, E-cadherin of MCF-7 cells. Conclusions Digoxin combined with tamoxifen can synergistically inhibit the proliferation, migration, invasion and induce apoptosis of MCF-7 cells, the possible mechanism of which may involve the suppression of PI3K-Akt signaling pathway and epithelial-mesenchy-mal transition (EMT).
