2-methoxyestradiol induces apoptosis and cell cycle arrest in human chondrosarcoma cells.
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.
Fong
Yi-Chin
YC
China Medical University Hospital, Taichung, Taiwan.
Yang
Wei-Hong
WH
Hsu
Sheng-Feng
SF
Hsu
Horng-Chaung
HC
Tseng
Kuo-Fung
KF
Hsu
Chin-Jung
CJ
Lee
Chun-Yi
CY
Scully
Sean P
SP
D000077584:2-Methoxyestradiol; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000187:drug effects / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects*; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D019902:Chondrocytes / Q000187:drug effects; D002813:Chondrosarcoma / Q000188:drug therapy*; D045304:Cytochromes c / Q000187:drug effects / Q000378:metabolism; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology; D005434:Flow Cytometry; D006801:Humans; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000187:drug effects / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000187:drug effects / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D004958:Estradiol; D000077584:2-Methoxyestradiol; D045304:Cytochromes c; D053148:Caspase 3