Differential pro-apoptotic effect of allicin in oestrogen receptor-positive or -negative human breast cancer cells

Abstract

Allicin is known to induce apoptosis and inhibit tumourigenesis in various carcinoma cells. However, the precise mechanism of allicin-induced apoptosis remains unclear in human breast cancer cells. Here we found that ERα−MDA-MB-231 cells were more sensitive to allicin-induced apoptosis as compared with ERα+MCF7 cells. We also found that allicin induced reactive oxygens species (ROS)-mediated and caspase-dependent apoptosis in MDA-MB-231 cells, but not in MCF7 cells. Additionally, we showed the p38 and JNK pathways were involved in allicin-induced apoptosis. Furthermore, we demonstrated that ERα-knockdown increased cell growth suppression and apoptosis of MCF7 cells in response to allicin, whereas ERα-overexpression decreased cell growth suppression and apoptosis of MDA-MB-231 cells, implicating that ERα has a protective role during allicin-induced apoptosis. Collectively, these findings suggest that allicin induces differential apoptotic pathways through MAPK activated by ROS-dependent or -independent signalling pathway in breast cancer cells.

Keywords

• Allicin
• Apoptosis
• Oestrogen receptor
• Breast cancer
• ER
• MAPK