Research Paper Volume 15, Issue 20 pp 11033—11051

Figure 3. SSH1 inhibition suppresses the viability, oncogenicity, and cancer stemness of HCC cells. (A) Representative western blot images and histograms comparing cell viability in THLE-2, Huh7-WT, Huh7-SSH1^-/-(1), and Huh7-SSH1^-/-(2) cells at 100x and 200x magnification. (B) Molecular structure of Sennoside A with a molecular weight of 862.74 g/dl. (C) Histograms of the cell viability of Huh7, HepG2, Mahlavu, or Hep3B cells treated with 0 - 100 μM Sennoside A for 24h or 48h, with IC₅₀ indicated. (D) Representative wound-healing migration images and histograms comparing the wound-gap closure in Huh7, Huh7-SSH1^-/-(1), Huh7-SSH1^-/-(2), 20 μM or 40 μM SenA-treated Huh7 cells. (E) Representative invasion assay images and histograms comparing the number of invaded Huh7, Huh7-SSH1^-/-(1), Huh7-SSH1^-/-(2), 20 μM or 40 μM SenA-treated Huh7 cells. (F) Representative colony-formation assay images and histograms comparing the number of colonies formed by Huh7, Huh7-SSH1^-/-(1), Huh7-SSH1^-/-(2), 20 μM or 40 μM SenA-treated Huh7 cells. (G) Representative tumorsphere-formation assay images and histograms comparing the number of tumorspheres formed by Huh7, Huh7-SSH1^-/-(1), Huh7-SSH1^-/-(2), 20 μM or 40 μM SenA-treated Huh7 cells. WT, wild type; SenA, Sennoside A; *p < 0.05; **p < 0.01; ***p < 0.001.