Figure 1.

Niclosamide treatment blocks the STAT3 signaling pathway and inhibits the cell growth of human esophageal cancer cell lines. (A) CE48T, CE81T and BE3 cells were treated with 10 µM niclosamide for 24 h, and the phosphorylation of Y705 and the total form of STAT3, as well as β-catenin, were investigated by western blot assay using β-actin as a loading control. (B) Cancer cells were seeded in 96-well plates and treated with a concentration series of niclosamide (0, 1.25, 2.5, 5, 10 or 20 µM) for 72 h, and then the relative cell viabilities were determined by MTS assay. Error bars represent the standard deviation. The viability of control cells was designated as 100%, and that of the other groups were expressed as the percent of the control. (C) Colony-forming ability of CE48T and BE3 cells analyzed by clone formation assay. Images of living cell clones indicated by the formation of dark-colored formazan dye by reduction of the tetrazolium salt MTS by metabolically active cells. STAT3, signal transducer and activator of transcription 3; MTS, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium.