For example, via regulating the Wnt/β-catenin axis, the elevated PLK4 accelerates colorectal cancer progression and induces epithelial-mesenchymal transition [47], which is similar to our findings, while conversely, PLK4 downregulation suppresses cell apoptosis, and underexpressed PLK4 is linked to unfavorable prognosis of hepatocellular carcinoma [48]. This evidence concerns the gene PLK4 and colorectal cancer.