Abstract |
2-Methoxyestradiol (2-ME) is an endogenous metabolite of 17β-estradiol. In this study, we determined the antitumour activities of 2-ME on the well-differentiated EC9706 esophageal carcinoma cells in vitro. 2-ME had a strong antiproliferative effect on EC9706 cells and caused an increase in the population of apoptotic cells, detected by flow cytometry. A significant number of cells were blocked in the G(2)/M phase of the cell cycle. 2-ME-treated cells demonstrated an increase in cyclin B1 and c-Myc protein levels, as well as an increase in the percentage of G(2)/M phase. Their up-regulation may be involved in 2-ME-induced apoptosis and G(2)/M cell cycle arrest of the EC9706 cells, and it precedes the onset of apoptosis.
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Authors | Bin Du, Zhilan Zhao, Huibin Sun, Sijia Ma, Jianwen Jin, Zhenzhong Zhang |
Journal | Cell biochemistry and function
(Cell Biochem Funct)
Vol. 30
Issue 2
Pg. 158-65
(Mar 2012)
ISSN: 1099-0844 [Electronic] England |
PMID | 22095881
(Publication Type: Journal Article)
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Copyright | Copyright © 2011 John Wiley & Sons, Ltd. |
Chemical References |
- Cyclin B1
- Proto-Oncogene Proteins c-myc
- Estradiol
- 2-Methoxyestradiol
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Topics |
- 2-Methoxyestradiol
- Apoptosis
(drug effects)
- Carcinoma
(drug therapy, genetics, metabolism, physiopathology)
- Cell Cycle
(drug effects)
- Cell Line, Tumor
- Cell Proliferation
(drug effects)
- Cyclin B1
(genetics, metabolism)
- Esophageal Neoplasms
(drug therapy, genetics, metabolism, physiopathology)
- Estradiol
(analogs & derivatives, pharmacology)
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Proto-Oncogene Proteins c-myc
(genetics, metabolism)
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