The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment

Yang Yang; Zhao Ying; Liao Wenjuan; Yang Jing; Zhu Weiguo

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The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment

Yang Yang 1 #,Zhao Ying 1,Liao Wenjuan 1,Yang Jing 1,Zhu Weiguo 2 *

1.Department of Biochemistry and Molecular Biology, Peking University Health Sciences Center

2.Department of Biochemistry and Molecular Biology, Peking University Health Sciences Center

*Correspondence author

#Submitted by

Subject:

Funding: 教育部博士点基金,国家自然科学基金（No.20070001800）

Opened online:31 March 2009

Accepted by: none

Citation: Yang Yang,Zhao Ying,Liao Wenjuan.The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment[OL]. [31 March 2009] http://en.paper.edu.cn/en_releasepaper/content/30933

Histone deacetylase (HDAC) inhibitors have been shown to induce cell cycle arrest and apoptosis in cancer cells. However, the mechanisms of HDAC inhibitor induced apoptosis are incompletely understood. In previous study, we found that HDAC inhibitor depsipeptide may induce apoptosis of human lung cancer cells through the forkhead box class O1 (FoxO1)-Bim pathway. In this study, we further explore the mechanisms of mediating FoxO1 after depsipeptide treatment in lung cancer cells. We found that depsipeptide-induced expression of Bim was directly dependent on acetylation of FoxO1 that is catalyzed by cAMP-responsive element-binding protein (CREB)-binding protein (CBP). Moreover, our results demonstrated that FoxO1 acetylation is required for the depsipeptide induced activation of Bim and apoptosis, using transfection with a plasmid containing FoxO1 mutated at lysine sites. These data show for the first time that a HDAC inhibitor induces apoptosis through the FoxO1 acetylation-Bim pathway.

Keywords:Depsipeptide;acetylation;FoxO1;Bim;apoptosis

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