Relationship between the inhibitory effect of fraxetin on breast cancer and estrogen signaling pathway.
- Author:
Hong-Nan HUO
1
;
Kun-Peng XIE
;
Li-Meng WANG
;
Ying JIANG
;
Wei ZOU
;
Ming-Jie XIE
Author Information
1. College of Life Science, Liaoning Normal University, Liaoning Provincial Key Laboratory of Biotechnology and Drug Discovery, Dalian 116081, China. E-mail: xmj1222@sina.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Breast Neoplasms;
metabolism;
Cell Proliferation;
Coumarins;
pharmacology;
Cyclin D1;
metabolism;
Estrogen Receptor alpha;
metabolism;
Estrogens;
pharmacology;
Humans;
MCF-7 Cells;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Signal Transduction
- From:
Acta Physiologica Sinica
2013;65(3):323-328
- CountryChina
- Language:Chinese
-
Abstract:
Estrogen signaling pathways play an important role in the regulation of the physiological function of breast cancer cell proliferation and apoptosis. The article used MTT assay, flow cytometer analysis and Western blot to detect the inhibition of fraxetin on MCF-7 cell cycle distribution and apoptosis, ERα, cyclin D1 and Bcl-2 expression levels, MAPK and PI3K signaling pathway to investigate the mechanism of anti-breast cancer of fraxetin. The results showed fraxetin inhibited E2β-stimulated MCF-7 cell proliferation in a dose- and time-dependent manner, reversed E2β-induced anti-apoptosis and promoted G0/G1 phase arrest. After treatment with fraxetin, the expression of ERα in MCF-7 cell was decreased, and estrogen genomic signaling pathway was inhibited by down-regulating the expression of cyclin D1 and Bcl-2 proteins. After MCF-7 cells were treated with fraxetin, the expressions of MAPK/Erk1/2 protein were reduced, which affected estrogen non-genomic signaling pathway. The results suggest fraxetin plays a part in anti-breast cancer function through E2β-mediated genomic and non-genomic signaling pathways.
