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. 2015 Oct 20;7(1):351–361. doi: 10.18632/oncotarget.5968

Figure 2. hTERTpromotes EMT independent of the Wnt signaling pathway.

Figure 2

A. Colorectal cancer cells were co-transfected with 100 nM hTERT plasmid and a TOP-FLASH reporter (0.1 ng/well in each 96-well plate), and Wnt signal agonists(LiCl) and inhibitor(XAV) were added TOP-FLASH reporter activation was tested 48 h later. A scrambled construct was used as a negative control (NC). *P < 0.05 compared to control. B. Western blot of E-cadherin in HCT116 and SW480 cells(Lane1, No treatment; Lane2, hTERT overexpression; Lane3, Wnt inhibition; Lane4, hTERT overexpression plus Wnt inhibition). C–D. Colorectal cancer cells were co-transfected with 100 nM hTERT plasmid and a luciferase reporter containing the E-cadherin promoter (0.1 ng/well in each 96-well plate), and luciferase activity was tested 48 h later. A scrambled construct was used as a negative control (NC). *P < 0.05 compared to control. (C) The relative luciferase activity of the E-cadherin promoter in HCT116 cells. (D) The relative luciferase activity of the E-cadherin promoter in SW480 cells.