Open AccessApoptotic protease activating factor‐1 negatively regulates Wnt signaling in hepatocellular carcinoma
Author(s) -
Han Rui,
Chen XinYi
Publication year - 2019
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12089
Subject(s) - wnt signaling pathway , viability assay , apoptosis , cell cycle , cancer research , transfection , catenin , gene silencing , signal transduction , microbiology and biotechnology , medicine , cell culture , biology , biochemistry , gene , genetics
Abstract 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.