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. 2016 Jul 18;7(33):53191–53203. doi: 10.18632/oncotarget.10668

Figure 3.

Figure 3

(A) Time course treatment of CX-4945 at 10 μm decreases β Catenin protein as early as 10 min in western blot analysis in MPNST (S462-TY) cells. (B) Partial rescue of CX-4945 MPNST cytotoxicity is achieved by inhibiting GSK-3β through CHIR99021 or LiCl as measured through MTS assay 72 h. post treatment; y-axis is O.D. reading at 490 nm. (C) Treatment with GSK-3β inhibitors restored β Catenin protein in CX-4945 treated MPNST cells (24 h) as measured by western blot analysis. (D) Treatment with GSK-3β inhibitors restored β-Catenin target gene mRNA expression in CX-4945 treated MPNST cells (24 h) as measured by qPCR. (E) Western blot shows that shCTNNB1 induces apoptosis (cleaved PARP) in MPNST cells (S462-TY). (F) MPNST (S462-TY) cells treated with shRNA containing a non-targeting sequence or against β-Catenin and then stained with propidium iodide. Flow analysis of these samples reveals no significant difference in the cell cycle profile. (S.D. of NT = 1.6% and shCTNNB1 = 5.3%). Western blot above the cell cycle analysis shows that the shRNA effectively targeted β-Catenin. Asterisks indicate statistically significant differences (*p < 0.05, **p < 0.01, ***p < 0.001); Student's t-test. MTS and qPCR results are the mean of three independent biological replicates each in triplicate ± S.D.