Ginsenoside CK suppressed TNFα-stimulated EMT of HCC in vitro. (A) HCC-LM3, SMMC-7721 and HepG2 cell lines were treated with 5 and 10 μM CK in the absence or presence of 20 ng/mL TNFα for 24 h. HIF-1α, EMT related proteins and cytokines, IκBα and p-IκBα were assessed by Western blot analysis. (B) SMMC-7721 cells were treated with 5 and 10 μM CK in the absence or presence of 20 ng/mL TNFα for 24 h. The immunofluorescence staining of IκBα (red), p-IκBα (red) and vimentin (red) is presented. DAPI (blue) was used to mark the cell nuclear. Magnification 400×. (C) HCC-LM3 cells were treated with ginsenoside CK in the absence or presence of CoCl2 and TNFα. HIF-1α, EMT related proteins, IκBα and p-IκBα were assessed by Western blot analysis. Quantification plots are shown below. Data were shown as mean ± SD (n = 3). * p < 0.05, ** p < 0.01 compared with untreated control cells. # p < 0.05, ## p < 0.01 vs. TNFα-treated group. The figures shown were representative of three independent experiments.