Purpose: This study was undertaken to investigate the anticancer effects of Sulforaphane against liver cancer and to elucidate the underlying molecular mechanisms.
Methods: WST-1 assay was used to monitor the proliferation rate. DAPI and annexin V/propidium iodide (PI) staining was used for apoptosis. Flow cytometry was used for cell cycle analysis. Wound heal and transwell assays were used to monitor cell migration and invasion. The protein expression was determined by western blot analysis.
Results: It was found that Sulforaphane decreased the viability of the liver cancer HepG2 cells and exhibited an IC50 of 9 µM. Nonetheless, Sulforaphane (µM) exerted very low toxic effects on the normal AML12 hepatocytes and exhibited an IC50 of 100 µM. Flow cytometery analysis showed that Sulforaphane triggered G2/M arrest of the liver HepG2 cancer cells. DAPI staining revealed that Sulforaphane triggered the apoptotic cell death of HepG2 cells which was accompanied with activation of caspases 3 and 9, upregulation of Bax and downregulation of Bcl-2. Transwell assays showed that Sulforaphane inhibited the migration and invasion of the HepG2 liver cancer cells in a dose dependent manner. The effects of Sulforaphane were also investigated on the MAPK7 signalling pathway and it was found that Sulforaphane could block this pathway in HepG2 cells.
Conclusion: Taken together, Sulforaphane may prove essential in the development of chemotherapy for liver cancers.