Loading...
|
Please use this identifier to cite or link to this item:
http://ntur.lib.ntu.edu.tw/handle/246246/2006111501222388
|
| Title: | Goniothalamin induces cell cycle-specific apoptosis by modulating the
redox status in MDA-MB-231 cells |
| Authors: | Chen, Wen-Ying;Wu, Chin-Chung;Lan, Yu-Hsuan;Chang, Fang-Rong;Teng, Che-Ming;Wu, Yang-Chang |
| Contributors: | National Taiwan University Coll Med |
| Keywords: | Goniothalamin;Redox status;cdc25C;Apoptosis;MDA-MB-231 cell |
| Date: | 2005 |
| Issue Date: | 2006-11-15 |
| Abstract: | Goniothalamin, a natural occurring styryl-lactone, is a novel compound with putative anticancer activities. In the present study, the mechanism
of action of goniothalamin was further investigated in human breast cancer MDA-MB-231 cells. Goniothalamin treatment of cells significantly
induced cell cycle arrest at G2 /M phase and apoptosis. By means of cell cycle synchronization, the G2 /M phase cells proved to be the most
sensitive fraction to goniothalamin-induced apoptosis. Cells treated with goniothalamin revealed an increase in intracellular reactive oxygen
species and a decrease in intracellular free thiol contents. The disruption of intracellular redox balance caused by goniothalamin was associated an
enhancement of cdc25C degradation. Furthermore, the antioxidant N-acetylcysteine and the glutathione synthesis inhibitor DL-buthionine-(S, R)-sulfoximine,
inhibited and enhanced, respectively, the effects of goniothalamin on cell cycle arrest and apoptosis. Taken together, our result
demonstrates for the first time that goniothalamin disrupts intracellular redox balance and induces cdc25C degradation, which in turn causes cell
cycle arrest and cell death maximally at G2 /M phase in MDA-MB-231 cells. |
| Relation: | European Journal of Pharmacology 522,20-29 |
| Appears in Collections: | [College of Medicine] Periodical Articles
|
Files in This Item:
| File |
Description |
Size | Format | |
|---|
| 2329.pdf | | 391Kb | Adobe PDF | 130 | View/Open |
|
All items in NTUR are protected by copyright, with all rights reserved.
|
