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

2009 Fiscal Year Final Research Report

• Project/Area Number: 20790722
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Single-year Grants
• Research Field: Pediatrics
• Research Institution: University of Yamanashi
• Principal Investigator: SATO Hiroki University of Yamanashi, 大学院・医学工学総合研究部, 医学研究員 (70422681)
• Project Period (FY): 2008 – 2009
• Keywords: 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

Research Abstract

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.