Fig. 5: RNA sequence analysis of MOLM-13 cells treated with APG-115, AZA, Ara-C, or combinations as indicated for 24 h. | Cell Death Discovery

Fig. 5: RNA sequence analysis of MOLM-13 cells treated with APG-115, AZA, Ara-C, or combinations as indicated for 24 h.

From: MDM2 inhibitor APG-115 exerts potent antitumor activity and synergizes with standard-of-care agents in preclinical acute myeloid leukemia models

Fig. 5

MOLM-13 cells treated with APG-115 (40 nM), AZA (3 μM), Ara-C (100 nM), alone or in combination for 24 h in triplicates. Cells were collected for RNAseq analysis after treatment. A, B Numbers of differentially expressed genes after each treatment. C, D The most significantly enriched biological processes upregulated or downregulated in response to combined treatments: both AZA and Ara-C together with APG-115 upregulated P53, while the APG-115-AZA combination more markedly downregulated AML cell cycle, DNA replication, and mismatch repair. E, F Representative differentially expressed genes in response to APG-115, AZA, or Ara-C, alone or in combination. Combinations of APG-115 with either agent upregulated genes encoding the P53 pathway and downregulated those related to the cell cycle pathway, but only the APG-115-AZA combination markedly downregulated genes implicated in DNA repair. Expression levels are presented as normalized log2 counts per million. BBC3 Bcl-2-binding component 3 gene, CCNB1 Cdc2-cyclin B1 gene, DMSO dimethylsulfoxide vehicle, CDC20 cell division cycle 20 gene, CDKN1A cyclin-dependent kinase inhibitor 1A gene, GADD45 growth arrest and DNA damage-inducible 45, GDF15 growth differentiation factor 15 gene, KEGG Kyoto Encyclopedia of Genes and Genomes, MCM2/4 minichromosome maintenance proteins 2/4 gene, PLK-1 serine/threonine-protein kinase (also termed Polo-like kinase 1) gene, SESN1/2, sestrin 1 and 2 genes.

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