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Apoptotic protease activating factor‐1 negatively regulates Wnt signaling in hepatocellular carcinoma

The current study aims to evaluate the mechanism of apoptotic protease activating factor‐1 (Apaf‐1) in hepatocellular carcinoma (HCC) cells by verifying the regulation of the wnt/beta‐catenin signaling pathway via Apal‐1. Our data showed that transfection with Ad‐Apaf‐1 could inhibit the activity of a lymphoid enhancer factor (LEF) luciferase plasmid activated by β‐catenin. Overexpressing Apaf‐1 could suppress the β‐catenin‐induced LEF luciferase activity in a dose‐dependent manner. Western blot assays demonstrated that the overexpression of Apaf1 significantly suppressed the expression of Wnt/β‐catenin signaling‐related proteins. Further study demonstrated that Apaf‐1 suppressed HepG2 cell migration, invasion, and viability. Knocking down the expression of Apaf‐1 activated the wnt/β‐catenin pathway in HepG2 cells. In contrast, silencing β‐catenin decreased the activation of wnt/β‐catenin, even in the presence of si‐Apaf‐1. Cell cycle distribution analysis demonstrated a decrease in the number of cells in the G0/G1 phase in the Apaf‐1 silencing group. In contrast, knocking down the expression of β‐catenin increased the number of cells in the G0/G1 phase, even in the presence of si‐Apaf‐1. In summary, the Apaf‐1‐mediated suppression of HepG2 cell malignancy is achieved by inhibiting the wnt/β‐catenin pathway.