Abstract
Curcumin (C21H20O6) is considered to exert anticancer potential. However, the relationship between curcumin and β-catenin has not been fully clarified and its regulatory role in human liver cancer has not yet been confirmed. In this study, human liver cancer cells were exposed to curcumin and the proliferation of HepG2 cells was detected by MTT method along with analysis of cell cycle and apoptosis, as well as Wnt/β-catenin signaling proteins expression. Curcumin shows a time-dependent and dose-dependent effect on HepG2 cell proliferation. The IC50 at 24 h, 48 h and 72 h were 12.8±0.67) μmol/L, 8.8±0.43 μmol/L and 4.6±0.42 μmol/L, respectively. Curcumin could dose-dependently (5, 10 and 20 μmol/L) arrest HepG2 cells in the G2/M phase (p < 0.05) and increase apoptosis (p < 0.05). In addition, curcumin down-regulated total, cytoplasmic and nuclear β-catenin proteins in HepG2 cells, indicating inhibited Wnt/β-catenin signaling. Curcumin reduced the expression of Dvl-2, Dvl-3, GSK-3β (p-ser9), C-myc, and Survivin, and increased the expression of GSK-3 (p-tyr216) and Axin-2 without affecting total GSK-3β levels. Curcumin is able to inhibit liver cancer cell activities possibly through inhibition of Wnt/β-catenin signaling.
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