Emodin induces apoptosis of cancer cells and inhibits retinoid X receptor transcriptional activity.
- Author:
Fu-Lin HE
1
;
Li WANG
;
Xiao-Kun ZHANG
;
Jing-Zhang ZENG
Author Information
1. Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200233, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Dose-Response Relationship, Drug;
Emodin;
metabolism;
pharmacology;
Humans;
Retinoid X Receptor alpha;
metabolism;
Signal Transduction;
drug effects;
Transcriptional Activation;
drug effects;
Tretinoin;
antagonists & inhibitors
- From:
Acta Pharmaceutica Sinica
2008;43(4):350-355
- CountryChina
- Language:Chinese
-
Abstract:
The mechanisms by which emodin induces apoptosis and inhibits proliferation of cancer cells remain unclear. In this study, we investigated whether the proapoptotic effect of emodin on human NIH-H460 lung cancer cells and SMMC-7721 liver cancer cells was related to regulating RXR expression and function. MTT assay and DAPI staining were used to detect the anti-proliferative and apoptotic effects of emodin with or without 9-cis-retinoid acid on H460 and SMMC-7721. The reporter assay was used to detect the effect of emodin on RXR homo- and hetero-dimer transactivation. Competitive ligand binding assay was carried out to detect whether emodin could directly bind to RXR. The result showed that emodin could strongly inhibit the proliferation and induce apoptosis of both cancer cell lines, which could be antagonized by 9-cis-RA. The reporter assay showed that emodin could inhibit the transcriptional effect of the homo- and hetero-dimer transactivation of RXRalpha dose-dependently. However, in vitro binding assay did not show that emodin bind to RXRalpha-LBD directly. The findings suggest that exhibition of emodin its anti-cancer activity may be associated with involvement of RXRalpha signal transduction pathways.
