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Fig. 6 | Molecular Cancer

Fig. 6

From: CircRNF220, not its linear cognate gene RNF220, regulates cell growth and is associated with relapse in pediatric acute myeloid leukemia

Fig. 6

MiR-30a partially rescues circRNF220 function. A Illustration of miRNA-binding sites in circRNF220; miRNAs predicted to interact with circRNF220 are highlighted in orange. B Correlation between circRNF220 and miR-30a levels. C The miR-30 family expression levels in siRNA-circRNF220 were determined by qPCR in primary AML cells. D RNA pulldown using biotinylated circRNF220 and detection of miRNAs in primary AML cells. U6 was used as the control. Plots with error bars show the mean ± SD from triplicates unless otherwise stated. E Abundances of circRNF220, BIM, ELK3, IER2, GLUD2, and MYSM1 upon overexpression of miR-30a in primary AML cells. GAPDH was used as the control. F Abundances of BIM, ELK3, IER2, GLUD2, and MYSM1 upon circRNF220 knockdown in primary AML cells. G Representative GSEA plots showing the most strongly downregulated miR-30 targets (NES = -1.27, FDR < 0.001) in primary AML patient cells treated with LV-sh-circRNF220. The results were compared with those in AML patient cells treated with LV-siRNA-NC. H Relative transcript levels of miR-30 target mRNAs in AML patient cells and normal control cells, normalized to GAPDH transcript levels. The heatmap indicates the average of three independent experiments. I-J Cell proliferation decreased upon miR-30a OE and was rescued after circRNF220 overexpression in HL-60 (I) and K562 cells (J). The data are presented as the mean values of triplicates. K Cell apoptosis upon miR-30a mimics and rescued after circRNF220 overexpression in HL-60 cells. The numbers indicate the percentages of apoptotic HL-60 cells. Data represent mean value from triplicates. HC, healthy control; P (CR), primary patient with complete remission; P (Re), primary patient with relapse; CR, complete remission; Re, relapse; * P < 0.05, **P < 0.01, *** P < 0.001. ns: not significant

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