Paired ChIP-Seq studies of Kasumi-1 t(8;21) AML cells

Nearly 10-15% of all acute myeloid leukemia (AML) cases are caused by a recurring chromosomal translocation between 8 and 21, t(8;21). The t(8;21) translocation generates the AML1-ETO leukemia fusion protein. AML1-ETO promotes leukemogenesis by transcriptionally dysregulating important cell-fate genes. Here, to better understand how AML1-ETO deregulates transcription, we performed paired ChIP-Seq analyses of sequence-specific transcription factors, coactivators, corepressors, HDACs, RNA Pol II and acetyl-histone marks in both control and AML1-ETO-depleted Kasumi-1 t(8;21) AML cells. Chromatin immunoprecipitation using specific antibodies followed by deep sequencing in Kasumi-1 t(8;21) AML cells.

约10%至15%的急性髓系白血病（acute myeloid leukemia, AML）病例由8号与21号染色体间的复发性染色体易位t(8;21)所导致。该t(8;21)易位会生成AML1-ETO白血病融合蛋白。AML1-ETO可通过转录失调关键细胞命运基因，促进白血病发生发展。为深入解析AML1-ETO调控转录的分子机制，本研究对对照组与AML1-ETO敲降的t(8;21)型急性髓系白血病Kasumi-1细胞，开展了序列特异性转录因子、辅激活因子、辅阻遏因子、组蛋白去乙酰化酶（Histone Deacetylases, HDACs）、RNA聚合酶II（RNA Polymerase II, RNA Pol II）以及乙酰化组蛋白标记物的配对染色质免疫共沉淀测序（Chromatin Immunoprecipitation Sequencing, ChIP-Seq）分析。本研究采用特异性抗体进行染色质免疫共沉淀，随后对t(8;21)型急性髓系白血病Kasumi-1细胞开展深度测序。