期刊
CURRENT MEDICINAL CHEMISTRY
卷 20, 期 12, 页码 1609-1619出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/0929867311320120010
关键词
Bisacylimidoselenocarbamates; CDK1; Chk2; G2/M cell cycle arrest; MCF-7 breast cancer cells
资金
- Ministerio de Ciencia e Innovacion from Spain [SAF 2009-07744]
- Departamento de Industria, Gobierno de Navarra
- Departamento de Educacion, Gobierno de Navarra
- CAN Foundation
Bisacylimidoselenocarbamate derivatives (BSC) are potent anticancer agents with a strong cytotoxic activity against different types of tumour cells. Based in phosphatidylserine exposure on the cell membranes we show that BSC treatment resulted in enhanced cell death in leukaemia CCRF-CEM cells. DNA fragmentation detection in breast adenocarcinoma MCF-7 cells showed that BSC triggered cell death is concentration and time dependent. We also show that two of these compounds, BSC 3g and 3n, cause cell-cycle arrest in the late G2/M in MCF-7 cells. Consistent with this, a reduction in CDK1 and CDK2 expression with no change in cyclin A an B1 was observed in this cell line. Activation of caspase-2 was also detected. However, the involvement of the caspase-dependent pathway in the process of cell death induced by either BSC 3g or 3n is discarded since cell death could not be prevented by pretreatment with the pancaspase inhibitor z-VAD-fmk. Moreover, since reduced levels of p21(CIP1) and Chk2 proteins but no change in p53 levels could be detected in MCF-7 cells after BSC 3g or 3n treatment our results suggest that BSC treated cells die from lethal mitosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据