急性髓系白血病（AML）是一类恶性血液肿瘤疾病，其临床治疗策略目前仍依靠化疗药物对肿瘤细胞进行杀伤。AML细胞对于常规化疗药物的耐受能力一直是该类疾病治疗中的主要障碍。阿糖胞苷作为AML化疗过程中所采用的一线药物，其使用距今已经有数十年的历史，而肿瘤细胞对于该药物的耐受机制仍有很多不确定的因素。为探究这一问题，我们选用急性髓系白血病细胞系THP-1作为研究对象，利用基于CRISPR/Cas9技术的全基因组敲除筛选技术对THP-1细胞系进行阿糖胞苷耐药基因的筛选。通过分析筛选得到测序数据，我们锁定SUMO3作为细胞阿糖胞苷耐药表型的负责基因，并将深入挖掘SUMO化修饰底物同阿糖胞苷耐药表型之间的具体生化机制，为新的药物开发提供研究思路和治疗靶点。

Acute myeloid leukemia (AML) is a form of blood cancer that is characterized with myeloid cells unlimited proliferation. The current therapy strategy relies on chemical drugs to kill the tumor cells. Although most chemical works well at the first time, the followed drug resistance become the main barrier of complete response. Cytarabine(Ara-C) has been one of the cornerstone drugs in the treatment of acute myeloid leukemia (AML) for more than three decades, but the resistance mechanisms of this medicine remains unclear. In this study, we will use genome-wide CRISPR library to screen the Ara-C resistance genes in the AML cell line THP-1. After analyzing the screening data, we identify SUMO3 as a potential target for THP-1 cell Ara-C resistance. We will try to find the connection between Ara-C resistance and cell sumoylation network, and characterize the sumoylated protein involved in Ara-C resistance pathway, to discover potential targets for specific drug designing.