Apigenin suppresses colorectal cancer cell proliferation, migration and invasion via inhibition of the Wnt/β-catenin signaling pathway

Abnormal activation of the Wnt/beta-catenin signaling pathway has a significant role in human tumorigenesis. The search for potential anticancer drugs has included widespread screening of inhibitors of the Wnt signaling pathway. Recently, one of the most common flavonoids, apigenin, demonstrated potential anti-tumor effects on multiple human cancer cell lines, with low cytotoxicity and no mutagenic activity. However, the association between apigenin and the Wnt/beta-catenin signaling pathway remains to be elucidated. The results of wound healing and Transwell invasion assays revealed that apigenin was able to significantly suppress colorectal cancer cell proliferation, migration and invasion in a dose-dependent manner. An organoid culture assay revealed that apigenin was also able to suppress the growth of intestinal organoids. Furthermore, apigenin inhibited beta-catenin/T-cell factor/lymphoid enhancer factor signaling activation, which was induced by LiCl in a dose-dependent manner. This inhibited beta-catenin nuclear entry, and therefore the expression of Wnt downstream target genes. In conclusion, apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth by inhibiting the Wnt/beta-catenin signaling pathway.