Fig. 7. CpG-M-miR-142 sensitizes BC CML to TKIs.

a–c Experimental design and results. a A cohort of BC CML mice were generated by transplanting 10⁶ BM MNCs from diseased miR-142^−/−BCR-ABL mice (CD45.2) into congenic wt recipient mice (CD45.1). At 2 weeks post transplantation, these mice were treated with CpG-M-miR-142 (20 mg/kg/day, IV), NIL (50 mg/kg/day, gavage), CpG-M-miR-142 + NIL, or SCR + NIL for 3 weeks. b WBC counts, PB engraftment rates, and survival (n = 10 mice per group). c WBC counts, PB engraftment rates, and survival of the 2nd recipient mice transplanted with BM MNCs from the treated donors (n = 10 mice per group). d–f Experimental design and results. d BC CML PDX mice were generated by transplanting 2 × 10⁶ CD34⁺ cells from BC CML patients into NSG mice. Upon detecting >5% human CD45⁺ cell engraftment in PB, these PDX mice were treated with CpG-M-miR-142 (20 mg/kg/day, iv) + NIL (50 mg/kg/day, oral garage) or SCR + NIL for 3 weeks. e PB and BM engraftment rates and survival (n = 10 mice per group). f PB engraftment rates and survival of the 2nd recipients transplanted with BM MNCs from the treated donors (n = 10 mice per group). For b, c and e, f, source data are provided as a Source Data file. M-miR-142 CpG-M-miR-142, NIL Nilotinib, SCR CpG-scramble miRNA control, WBC white blood cell, PB peripheral blood. Comparison between groups was performed by two-tailed, unpaired t-test. Survival curves were compared by Log-rank test. Results shown represent mean ± SEM.