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Differential mechanism of HDACI induct cell cycle arrest, apoptosis and differentiation between B-precursor and T-lineage leukemia cells

Differential mechanism of HDACI induct cell cycle arrest, apoptosis and differentiation between B-precursor and T-lineage leukemia cells
HDACI诱导B前体和T系白血病细胞周期阻滞、凋亡和分化的差异机制
批准号：
20790722
负责人：
SATO Hiroki
金额：
$2.75万
依托单位：
University of Yamanashi
依托单位国家：
日本
项目类别：
Grant-in-Aid for Young Scientists (B)
财政年份：
2008
资助国家：
日本
项目状态：
已结题
起止时间：
2008 至 2009
来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20790722/
关键词：
小児血液学シグナル伝達アポトーシス細胞周期停止HDAC inhibitor

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中文摘要
翻译
我们在白血病细胞系中加入HDAC抑制剂TSA。并分析了TSA诱导白血病细胞系凋亡和细胞周期停滞的作用。我们使用B-前体ALL和T系ALL，并分析了它们之间的差异。诱导细胞凋亡时，Bim在B系ALL中表达上调，PUMA在T系ALL中表达上调。在细胞周期停滞方面，认为p21与B系ALL的G0/G1期停滞有关，CDC25C、CDC2和细胞周期蛋白与T系ALL的G2/M期停滞有关。
英文摘要
We added TSA which was HDAC inhibitor in Leukemia cell lines. And we analyzed TSA induced apoptosis and cell cycle arrest in Leukemia cell lines. We used B-precursor ALL and T-lineage ALL, and analyzed difference of each other. When apoptosis was induced, Bim was up-regulated in B-precursor ALL and PUMA was up-regulated in T-lineage ALL. About cell cycle arrest, it was suggested p21 associated with G0/G1 arrest in B-precursor ALL, and CDC25C, CDC2, and cyclins contribute G2/M arrest in T-lineage ALL.
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