Mechanism of Icariin induces mitochondrial-mediated apoptosis by Wnt/β-catenin signaling pathway in colorectal cancer.

BACKGROUND

To evaluate the effect of Icariin (ICA) on AOM/DSS-induced colorectal cancer (CRC) in mice as well as CRC cells, and to explore the underlying molecular mechanism.

METHODS

The therapeutic efficacy of ICA against AOM/DSS-induced CRC was evaluated by detecting tumor growth and pathological alterations. Biomarkers related to Wnt/β-catenin and mitochondrial apoptosis were tested, and cell experiments were performed to validate the regulatory correlation between ICA and the Wnt/β-catenin pathway in CRC cells.

RESULTS

ICA significantly reduced tumor number, size and ameliorated pathological damage in AOM/DSS-induced mice by regulating the mitochondrial-mediated apoptosis of colon tissue. ICA's regulation of mitochondrial-mediated apoptosis was confirmed to involve the Wnt/β-catenin signaling pathway. In vitro, ICA restrained proliferation, migration and invasion of SW1463 and HCT116 cells, decreased mitochondrial membrane potential and changed the expression of pathway-related genes.

CONCLUSION

The study demonstrated that ICA promoted mitochondrial-mediated apoptosis by regulating the Wnt/β-catenin signaling pathway, suggesting that ICA could serve as a potential treatment for CRC.