Abstract | BACKGROUND: Multi-drug resistance to chemotherapeutic agents is a major cause of treatment failure in breast cancer. In this study, we investigated the effects of emodin on reversing the multi-drug resistance, examined the ERCC1 protein expression in breast cancer cell line, and explored the relationship between reversal of multi-drug resistance and ERCC1 protein expression. METHODS: MTT assay was conducted to test the cytotoxicity of adriamycin and cisplatin to MCF-7/Adr cells with and without emodin pretreatment, and Western blot was performed to examine the ERCC1 protein expression. RESULTS: MCF-7/Adr cells had 21-fold and 11-fold baseline resistances to adriamycin and cisplatin, respectively. When emodin was added to the cell culture at the concentration of 10 μg/ml, the drug resistance was reduced from 21 folds to 2.86 folds for adriamycin, and from 11 folds to 1.79 folds for cisplatin. MCF-7/Adr cells treated with two concentrations (10 μg/mL and 20 μg/mL) of emodin, after 2, 4, 6, 10 days, the trend of ERCC1 expression was gradually decreased and the reduction was more obvious comparatively at the concentration of 20 μg/mL. CONCLUSIONS:
Emodin could reverse the multi-drug resistance in MCF-7/Adr cells and down-regulate ERCC1 protein expression.
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Authors | Jian-min Fu, Jie Zhou, Jian Shi, Jian-sheng Xie, Li Huang, Adrian Y S Yip, Wings T Y Loo, Louis W C Chow, Elizabeth L Y Ng |
Journal | Journal of translational medicine
(J Transl Med)
Vol. 10 Suppl 1
Pg. S7
(Sep 19 2012)
ISSN: 1479-5876 [Electronic] England |
PMID | 23046742
(Publication Type: Journal Article)
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Chemical References |
- DNA-Binding Proteins
- Doxorubicin
- ERCC1 protein, human
- Endonucleases
- Emodin
- Cisplatin
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Topics |
- Blotting, Western
- Breast Neoplasms
(metabolism, pathology)
- Cell Survival
(drug effects)
- Cisplatin
(pharmacology)
- DNA-Binding Proteins
(metabolism)
- Doxorubicin
(pharmacology)
- Emodin
(pharmacology)
- Endonucleases
(metabolism)
- Female
- Humans
- Inhibitory Concentration 50
- MCF-7 Cells
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