Allicin suppresses the migration and invasion in cervical cancer cells mainly by inhibiting NRF2

Emerging evidence has demonstrated the antitumor activity of allicin in various tumors. However, little study has been carried out on the functional role of allicin in cervical cancer. Our data showed that allicin suppressed cervical cancer cell viability in a time- and dose-dependent manner. Allicin treatment could reverse H(2)O(2)-induced reactive oxygen species accumulation. Meanwhile, levels of glutathione and superoxide dismutase were increased, but malondialdehyde was decreased after allicin incubation for 48 h. Furthermore, TUNEL staining showed that H(2)O(2) treatment induced cell apoptosis, but allicin treatment could decrease cell apoptosis. Western blot assay showed that allicin could suppress the expression of nuclear factor erythroid 2-related factor 2 (NRF2) and heme oxygenase 1. We also showed that NRF2 prompted SiHa cell proliferation and reduced SiHa cell apoptosis. More importantly, allicin-inactivated phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling could be partially reversed by overexpressing of NRF2. We also evaluated cell apoptosis in SiHa cells transfected with plasmid NRF2. Our data showed that allicin-induced cell apoptosis (43.5±3.8%) could largely be abolished by upregulation of NRF2 (12.3±2.08%). In summary, our data showed allicin was effective in suppressing the malignant phenotype of cervical cancer cells mainly by inhibiting the expression of NRF2, showing the potential clinical benefits of allicin in cervical cancer patients.