Fig. 3

Canonical Wnt signaling is inhibited by dinaciclib and combination treatment in primary AML samples. (A) mRNA expression of Wnt components GSK3β, AXIN2, CTNNB1, FZD1, and CDK14, canonical targets BIRC5, CCND1 and MYC, and the non-canonical target RAC1 in primary AML cells (n = 4–5 per gene) as measured by RT-qPCR. Results shown as mean ± SEM. (*, **, ***, **** = p ≤ 0.05, 0.01, 0.005, and 0.0001 respectively). (B) Immunoblots measuring total β-catenin protein levels from two primary AML samples (#9 and #10) after treatment with DMSO as vehicle control, dinaciclib (0.1 µM), PLX51107 (1 µM), combination dinaciclib and PLX51107, BML284, CHIR, or VP-16 (1 µM) for 24 h. BML284 and CHIR were chosen as positive activators of Wnt signaling and VP-16 was used as a standard cytotoxic agent