Inhibition of miR‐126 increases MDS‐L cell cycling and sensitizes cells to DAC treatment. A‐D. Relative miR‐126 expression level (A), cell cycling, as indicated by Ki‐67 staining (B), apoptosis, as indicated by Annexin V staining (C), and viability, as measured by luminescence assays (D) in MDS‐L miR‐126KD and control (Mock) cells. E‐F. Apoptosis, as indicated by Annexin V staining (E), and viability (F), based on luminescence assays, in MDS‐L miR‐126KD and control (Mock) cells exposed to DAC. (G) Experimental design was used to establish MDS‐L‐derived xenografts. NSGS mice were transplanted with MDS‐L cells to generate a cohort of mice. After engraftment was confirmed, mice were treated with SCR, miRisten (10 mg/kg/day, once a day), DAC (0.5 mg/kg/day, 3 times per week), or amiRisten/DAC combination for three wks. BM, PB, and SP cells were then harvested and analyzed. H: Representative flow cytometry plots of human CD45 cells (hCD45) in BM. I: BM hCD45 cell engraftment in mice bearing xenografted MDS‐L cells in‐vivo administrated with SCR, miRisten, DAC, or the miRisten/DAC combination (n = 5‐7 per group). Results shown represent mean± SEM. *P < 0.05, **P < 0.01, ***P < 0.001,****P < 0.0001; NS: not significant; by two‐tailed, paired Student's t‐test