USP20 promotes T-ALL evolution by deubiquitinating modified HIF1A

T-cell acute lymphoblastic leukemia (T-ALL) is a highly aggressive hematologic malignancy. The potential of investigating USP20 holds promise for more targeted therapies and better outcomes. Knocking down USP20 led to decreased T-ALL cell survival and growth both in vitro and in vivo, similar to using the USP20 inhibitor GSK2643943A. To explore USP20-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the USP20-knockdown J.gamma1 cells in comparison to control group. Cleavage Under Targets and Tagmentation (CUT&Tag) showed the co-localization of USP20 with HIF1a on chromatin in J.gamma1 cells. mRNA profiles of J.gamma1 cells transfected with control shRNA (sh-NC) or sh-USP20 were generated by RNA sequencing, in double, using Illumina NovaSeq6000. CUT&Tag using antibody against USP20 and HIF1a in J.gamma1 cells.