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.

我们在白血病细胞系中加入了HDAC抑制剂TSA。分析TSA诱导白血病细胞凋亡和细胞周期阻滞的作用。采用B前体细胞ALL和T细胞ALL，分析两者的差异。诱导细胞凋亡时，Bim在B-前体ALL中上调，而CD 44 A在T-系ALL中上调。在细胞周期阻滞方面，p21与B前体细胞ALL的G 0/G1期阻滞有关，而CDC 25 C、CDC 2和cyclins与T系细胞ALL的G2/M期阻滞有关。