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. 2021 Oct 5;12(10):908. doi: 10.1038/s41419-021-04209-2

Fig. 5. Increased double-stranded DNA breakage response and apoptosis may be a potential mechanism for miR-342-5p inhibition of CML.

Fig. 5

A The enrichment map presented divergent trends of GSEA enrichment with the treatment of 0.5 μM imatinib in miR-NEG or miR-342-5p expression. The width of the edge connected between nodes represents the degree of overlap, and similar nodes are auto-annotated as clusters. GSEA enrichment filtering criteria: P < 0.05, FDR < 0.25. B–E Western blot presents the expression of cell cycle components including CCND1 (B), Cell cycle regulating proteins (C), DNA repair components including ATM-chk2 and ATR-chk1 axis (D), and apoptosis-associated proteins (E) in K562 and MEG01 subjected to imatinib under miR-NEG or miR-342-5p expression (20 nM). F Validation of the effect of miR-342-5p on apoptosis in K562 caused by imatinib in the presence of miR-342-5p (20 nM) by Annexin-V/PI method using flow cytometry. The bar chart shows the difference in the percentage of cells at early apoptosis under duplication. The student’s t-test or One-way ANOVA approach was used to assess the significance. *P < 0.05; **P < 0.01; ***P < 0.001.