Fig. 2: D + E Selectively drives TP53 mutant myeloid tumor cell differentiation, leading to tumor regression.
a Xenograft establishment and drug administration: Xenografts (n = 6 per group) were established, and the indicated drugs were administered according to the flow diagram. b Comparative survival in TP53 KO MOLM13 and wide-type MOLM13 xenografts treated with D + E or saline, respectively. The data are presented as mean ± standard deviation. Significance levels are indicated as ***P < 0.001. c Quantification of bioluminescence: Using an in vivo imaging system and live-imaging software, the bioluminescence intensity was quantified and compared between D + E Group and PBS Control in MOLM13 xenografts and TP53 KO MOLM13 xenografts. d Morphological Analysis: SKM-1, THP-1, MOLM13, and TP53 KO MOLM13 cells were treated with indicated drugs for 5 days, followed by staining with Hank’s solution (×100 magnification). e Detection of CD11b expression and phagocytosis in TP53 Mutant (THP-1and SKM-1) and TP53 wide-type (MOLM13 and OCI-AML3) cell lines treated with indicated drugs for 3 or 5 days. f Detection of CD11b expression in CRISPR-Modified TP53 KO and Re-introduction in MOLM13 Cells (left part) as well as in THP-1 wide-type and TP53 overexpression clones treated with indicated drugs for 5 days. g Gene mutation detection and outcomes in patient-derived AML cells (left part) and detection of CD11b expression in these cells treated with indicated drugs for 5 days (right part). Data are expressed as mean ± standard deviation. Significance levels are indicated as *P < 0.05; **P < 0.01; ***P < 0.001. h Gene expression heatmap: This panel illustrates the expression levels of genes involved in cell differentiation and those maintaining cell stemness in gene-edited MOLM13 cells (Scramble, TP53 KO, TP53 KO + WT) treated with decitabine and/or etoposide.
