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Induction of Apoptosis and G2/M Cell Cycle Arrest by Oridonin in Human Gastric Cancer BGC-823 Cells
Jian Han #,Ye Min,Qiao Xue,Wu Wanying,Qu Guiqin,Guo Dean *
The State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University
*Correspondence author
#Submitted by
Subject:
Funding: 教育部(No.20040001136)
Opened online:14 December 2007
Accepted by: none
Citation: Jian Han,Ye Min,Qiao Xue.Induction of Apoptosis and G2/M Cell Cycle Arrest by Oridonin in Human Gastric Cancer BGC-823 Cells[OL]. [14 December 2007] http://en.paper.edu.cn/en_releasepaper/content/16926
 
 
The in vitro apoptosis-induction effects of oridonin on gastric tumor cells BGC-823 and its effects on cell cycle, mitochondrial membrane potential and intracellular Ca2+ were investigated to shed light on the mode of its anticancer action. The results showed that oridonin inhibited BGC-823 cells growth with IC50 of 22.21 μM. It induced apoptosis in a dose-dependent manner. In addition, it could decrease mitochondria membrane potential, increase intracellular Ca2+, and activate pro-caspase 3. BGC-823 cells were arrested in G2/M cell cycle phase with lower expression of cyclin A protein. The up-regulation of p53 was observed before apoptosis occurred and cell cycle arrest. It suggested that oridonin inhibits the proliferation of BGC-823 cells through G2/M cell cycle arrest and apoptosis induction, which is mediated by influx of Ca2+, up-regulation of p53, activation of caspase-3, and down-regulation of cyclin A.
Keywords:Oridonin; Human Gastric Cancer; Apoptosis; Cell cycle arrest; p53; cyclin A
 
 
 

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