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. 2016 Apr 20;7(24):36382–36394. doi: 10.18632/oncotarget.8871

Figure 1. Sp1 inactivation disrupted BCR/ABL signaling.

Figure 1

A. EMSA showing Sp1 binding on BCR/ABL promoter. The EMSA probes (hBCR1, hBCR2) covering Sp1 binding sites on BCR/ABL gene promoter were labeled by 32P and incubated with nuclear extract from K562 cells. The Sp1-DNA protein complex was competed with non-labeled corresponding probes (cold DNA). Note: n.s. cold DNA with TATA site. B-D. Modulation of Sp1/miR29b network altered BCR/ABL activities. K562 and KU812 cells were transfected with Sp1 siRNA for 48 hours, and subjected to Western blotting (B, D) or colony-forming assays (C). E. K562 cells were transfected with miR-29b for 48 hours and the cells were lysed for Western blotting. F. K562 and KU812 cells were treated with different doses of BORT for 24 hours and the cells were harvested for Western blotting. G. K562 cells were treated with BORT for 6 hours and subjected to colony-forming assays. The data represent three independent experiments; Data are mean ±SD; **p < 0.01, ***p < 0.001.