Fig. 2

XIST could competitively bind to miR-29a and up-regulate MYC expression. a The binding sites between miR-29a and XIST predicted by the online analysis. b The binding of miR-29a to XIST confirmed by dual luciferase reporter assay. c The relative expression of miR-29a in AML bone marrow samples determined by RT-qPCR (left); correlation between miR-29a and XIST analyzed by Pearson correlation analysis (middle); the expression of miR-29a in normal bone marrow mononuclear cells and KG-1 cells (right). d RIP was used to analyze the binding of AGO with XIST, MYC, miR-29a. e RNA pull down was used to analyze the binding of XIST with miR-29a. f RT-qPCR was used to determine the expression miR-29a in cells upon varied treatments. g The predicted binding sites between miR-29a and MYC. h Putative miR-29a binding site in the 3′UTR region of MYC confirmed by dual luciferase reporter assay. i RT-qPCR and Western blot analysis were used to determine the relative expression of MYC in AML bone marrow samples; correlation of XIST to MYC determined by Pearson correlation analysis (middle). j RT-qPCR and Western blot analysis were used to determine the relative expression of MYC in KG-1 cells. k RT-qPCR was used to determine the expression of MYC in cells overexpressing miR-29a. l RT-qPCR and Western blot analysis were used to determine the relative expression of MYC in cells with miR-29a knockdown. m RT-qPCR was used to determine the expression of XIST, miR-29a and MYC in cells upon varied treatments. n Western blot analysis was used to determine the protein expression of MYC in cells upon varied treatments. *p < 0.05 vs. KG-1 cells without any treatment. The data were measurement data, and expressed as mean ± standard deviation. Data comparison among multiple groups was conducted by one-way ANOVA. The experiment was repeated 3 times independently