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
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 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

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.

我们添加了TSA，该TSA是白血病细胞系中HDAC抑制剂。我们分析了TSA在白血病细胞系中诱导的凋亡和细胞周期停滞。我们使用了b-ecursor all and t-lineage，并彼此分析了差异。当诱导凋亡时，B-Exursor All中的BIM被上调，PUMA在T-Linege All中被上调。关于细胞周期停滞，建议与b-e-ecursor All中的G0/G1停滞有关的P21，CDC25C，CDC2和细胞周期蛋白在T-lineage中造成了G2/M的停滞。