Functional Analysis of ZFP91 in Myeloid Leukemia Cells to Identify EVI1 Expression Regulation
Ecotropic viral integration site 1 (EVI1) plays a crucial role in hematopoietic stem cell maintenance, and its overexpression is a poor prognostic factor in myeloid malignancies, including acute myeloid leukemia (AML). The incomplete understanding of EVI1 regulation and function, along with the absence of specific treatments for EVI1-overexpressing AML, highlights the need for new therapeutic strategies. Chromosomal rearrangements involving the EVI1 locus on 3q26.2 are associated with aberrant EVI1 expression, but many EVI1-high AML cases do not show such chromosomal abnormalities. The mechanisms behind EVI1 overexpression without chromosomal translocations remain unclear. In this study, we performed a genome-wide CRISPR/Cas9 knockout screen and identified zinc finger protein 91 (ZFP91) as a novel activator of EVI1. To further investigate the role of ZFP91 in regulating EVI1, we conducted RNA-seq on ZFP91 knockout (ZFP91-KO), EVI1 knockout (EVI1-KO) and control K562 cells, along with ChIP-seq and ATAC-seq on ZFP91-KO and control K562 cells. This bioproject contains the RNA-seq, ChIP-seq, and ATAC-seq data corresponding to these experiments.