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. 2019 Nov 25;20(23):5914. doi: 10.3390/ijms20235914

Figure 1.

Figure 1

Emetine inhibits the Wnt/β-catenin pathway, c-myc and cyclin D1 in human non-small cell lung cancer (NSCLC) cells. (A) The endogenous expression of total β-catenin in A549, CL1-0, CL1-5, H1299, H23, H358, and H647 human NSCLC cells was examined by Western blotting. β-Actin was used as the internal control. (B) CL1-0, CL1-5, A549, H1437, and H1355 human NSCLC cells were treated with or without 120 nM emetine for 48 hours. The protein expression of β-catenin, c-myc, and cyclin D1 was examined by Western blotting. β-Actin was used as the internal control. (C) The TOPflash (M50) reporter containing wild-type TCF/LEF binding sites produced a high level of transcriptional activity. The FOPflash (M51) reporter containing mutated TCF/LEF binding sites was used as the negative control. The relative luciferase activity of TOPflash/FOPflash was analyzed after 6 h of treatment with DMSO or the indicated concentration of emetine in the CL1-0 and H1437 cell lines. The data are expressed as the means ± SDs from three independent experiments. ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student’s t-test).