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. 2017 Jan 14;8(9):14604–14619. doi: 10.18632/oncotarget.14654

Figure 4. Effects of CK1 inactivation on β-catenin and AKT signalling pathways.

Figure 4

H929 (A), INA-6 grown alone or in co-culture with HS-5 (INA-6/HS-5) (B), CD138+ patient derived PCs grown alone or on patient-derived BMSCs or HS-5 (C) were treated with D4476 40 μM (H929 and patient PCs) or 20 μM (INA-6) for 48 h and the expression of phosphorylated β-catenin on Ser45 (p β-catenin S45), phospho β-catenin on Ser33/37/Thr41 (p β-catenin S33/37/T41), phospho AKT on Ser473 (p AKT S473), total β-catenin and AKT was evaluated by WB. GAPDH or α-tubulin was used as loading control. In C: 1 = MM#11, 2=co-culture of MM#12 on BMSC obtained from MM#28; 3 = co-culture of MM#12 on BMSC obtained from MM#8; 4 = co-culture of MM#12 on HS-5; 5 = co-culture of MM#20 on BMSC obtained from MM#28. The same analysis was performed in INA-6 (D, left panel) or H929 (E, left panel) cells electroporated with ds oligonucleotides against CK1α, in INA-6 wt or INA-6 CK1α shRNA#1 cellular clone treated with IPTG 500 μM for 1 week (D, middle and right panels) or in H929 wt, H929 CK1α shRNA#1 and shRNA#3 clones, treated with IPTG 500 μM (H929 wt and shRNA#1) or 1000 μM (shRNA#3) for 1 week (E, right panel).