Anticancer Effect of Polyphyllin I in Suppressing Stem Cell-Like Properties of Hepatocellular Carcinoma via the AKT/GSK-3β/β-Catenin Signaling Pathway

Figure 6

PPI affected the AKT/GSK-3β/β-catenin signaling pathway in LCSCs. (a) Western blotting was performed to compare the protein expression of β-catenin, NANOG, and OCT-4 in HCC cells and LCSCs. (b) PPI suppressed the protein expression of β-catenin, NANOG, and OCT-4 in LCSCs. (c) Immunofluorescence analysis was conducted to detect nuclear accumulation of β-catenin in PPI- and Sora-treated LCSCs. (d) A qPCR assay was conducted to examine the mRNA level of β-catenin in LCSCs after exposure to PPI. (e) β-catenin downregulation was triggered in the CHX group, while its degradation was remarkably facilitated in the CHX+PPI group. (f) The expression of β-catenin could not be downregulated by PPI whenMG132 was added. and vs. the control group; ^# and ^##vs. the MG132 group. (g) Western blotting demonstrated that PPI administration notably affected the main proteins of the AKT/GSK-3/β-catenin signaling pathway. (h) Western blotting indicated that PPI reversed the promoting effect of LiCl on the β-catenin level. The expression of β-catenin in the LCSCs was further decreased by PPI in the presence of LY (the AKT inhibitor) treatment. Meanwhile, inhibition of β-catenin by PPI is rescued by SC79 (the Akt activator). and vs. the control group; ^# and ^##vs. the Sora group.

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