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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
Fong et al. (Thu,) studied this question.