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2-methoxyestradiol induces apoptosis and cell cycle arrest in human chondrosarcoma cells

✍ Scribed by Yi-Chin Fong; Wei-Hong Yang; Sheng-Feng Hsu; Horng-Chaung Hsu; Kuo-Fung Tseng; Chin-Jung Hsu; Chun-Yi Lee; Sean P. Scully

Publisher
Elsevier Science
Year
2007
Tongue
English
Weight
378 KB
Volume
25
Category
Article
ISSN
0736-0266

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✦ Synopsis

Abstract

2‐Methoxyestradiol (2ME) is an endogenous metabolite with estrogen receptor‐independent anti‐tumor activity. The current study seeks to determine the mechanism of anti‐tumor activity of 2ME on human chondrosarcoma. 2ME caused a time‐ and dose‐dependent cytotoxity in chondrosarcoma cells, while primary chondrocytes were minimally affected. Cells accumulated in G0/G1 phase in response to 2ME and DAPI stain indicated an induction of apoptosis. Bax, Cytochrome C, and Caspase‐3 protein expression were increased, while p53 expression was decreased. A higher Bax/Bcl‐2 ratio followed 2ME treatment. 2ME has a potentially promising role as a systemic therapy of chondrosarcoma when the mechanism of action is better delineated. Published by Wiley Periodicals, Inc. J Orthop Res 25:1106–1114, 2007

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