Oenothein B inhibits proliferation and migration of breast cancer cells by regulating P53.
10.19540/j.cnki.cjcmm.20230413.702
- Author:
Mao-Hong LUO
1
;
Ya HE
1
;
Hong LI
1
;
Teng-Xiang CHEN
1
;
Shan LEI
1
;
Jin-Juan ZHANG
2
;
Lu WANG
1
Author Information
1. Department of Physiology, School of Basic Medical Sciences, Guizhou Medical University Guiyang 550025, China.
2. Functional Experimental Center, School of Basic Medical Sciences, Guizhou Medical University Guiyang 550025, China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
breast cancer cells;
migration;
oenothein B;
proliferation
- MeSH:
Humans;
Female;
Cell Proliferation;
Breast Neoplasms/drug therapy*;
Tumor Suppressor Protein p53/genetics*;
Molecular Docking Simulation
- From:
China Journal of Chinese Materia Medica
2023;48(14):3904-3912
- CountryChina
- Language:Chinese
-
Abstract:
The effects of oenothein B(OEB) on the proliferation, apoptosis, invasion, and migration of breast cancer MCF-7 and MDA-MB-231 cells were investigated by cell culture in vitro, network pharmacology, and molecular docking. In vitro cell experiments revealed that OEB inhibited the proliferation and colony formation ability, and promoted the apoptosis and formation of apoptotic bodies in breast cancer cells, as well as inhibited the invasion and migration of breast cancer cells. The targets of OEB were obtained using SwissTargetPrediction database and breast cancer targets were obtained from GeneCards. The targets of OEB and breast cancer were entered separately in Venny 2.1 software to obtain the Venn diagram of common targets of OEB and breast cancer. The common targets of OEB and breast cancer were input into STRING database to construct a protein-protein interaction(PPI) network, which was entered into Cytoscape 3.7.2 software for network topology analysis. Key targets were screened according to protein association strength, and analyzed for KEGG pathway enrichment. Molecular docking of OEB to key targets using AutoDock software revealed that OEB stably bound to the active pocket of P53, while OEB promoted the expression of P53 protein. MCF-7 and MDA-MB-231 cell viability and migration ability increased after silencing P53, and this change was reversed after treatment with OEB. Therefore, this study showed that OEB inhibited the proliferation, migration, and invasion of breast cancer MCF-7 and MDA-MB-231 cells, and promoted the apoptosis of breast cancer MCF-7 and MDA-MB-231 cells, which may be related to the targeted regulation of P53.
