Fig. 2

NK cells enhanced the anti-leukemia activity synergized with MCL1 inhibitor. a UMAP analysis of NK cells in AML samples at diagnosis and after chemotherapy by using single-cell RNA sequence data. The percentage of NK cells among them were further compared. b The flow cytometry analysis of BM infiltrated NK cells by CD45⁺CD3⁻CD56⁺CD16⁺ gating. c Proportions of lymphocytes and NK cells subsets in BM of patients with lymphoma, ND-AML and R/R AML. d The expression levels of KIRs in BM of patients with lymphoma, ND-AML and R/R AML. e Comparison of KIRs expression levels between high NK group and low NK group in ND-AML patients. f The cell viability test of OCI-AML3 and MOLM13 treated with venetoclax or maritoclax by co-cultured with UCB-NK cells. g Protein validation of the knockdown efficiency of MCL1 siRNAs in OCI-AML3 and MOLM13 cells. h-i The cell viability of OCI-AML3 and MOLM13 treated with MCL1 siRNA or scramble siRNA (h) and co-cultured with UCB-NK cells (i). j RNA and protein expression levels of BCL2 and MCL1 in normal controls and ND-AML samples with low or high NK cells. k Scheme of cell viability analysis by using primary samples of AML patients. l Cell viability of BM cells with high or low NK cells with venetoclax or maritoclax treatment. m-n Apoptosis induced by inhibitors among AML patient cells with high or low NK cells. Mean ± SEM values are shown. *P < 0.05, **P < 0.01, ***P < 0.001