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Fig. 5 | Experimental Hematology & Oncology

Fig. 5

From: The multi-CDK inhibitor dinaciclib reverses bromo- and extra-terminal domain (BET) inhibitor resistance in acute myeloid leukemia via inhibition of Wnt/β-catenin signaling

Fig. 5

Dinaciclib and combination treatment continues to inhibit Wnt signaling in BETi resistant and less sensitive cells. (A) mRNA expression of Wnt components and targets in MOLM-13, MV4-11, PLX51107 resistant MOLM-13, and PLX51107 resistant MV4-11 AML cells following 24-hour treatment with DMSO as vehicle control, dinaciclib (0.1 µM), PLX51107 (1 µM), or combination. Results are shown as mean ± SEM. (*, **, ***, **** = p ≤ 0.05, 0.01, 0.005, and 0.0001 respectively). (B) Immunoblots measuring protein levels of phosphorylated and total LRP6 in MV4-11 and PLX51107 resistant MV4-11 cell lines following treatment with vehicle, dinaciclib (0.1 µM), PLX51107 (1 µM), combination, or cytarabine (1 µM) for 24 h. (C) Representative immunoblots of MOLM-13 and PLX51107 resistant MOLM-13 AML cells measuring protein levels of β-catenin following 24-hour treatment with DMSO as vehicle control, dinaciclib (0.1 µM), PLX51107 (1 µM), combination, or cytarabine (1 µM)

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