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

• Published in: Journal of functional foods 2016-08, Vol.25, p.341-353
• Main Authors: Kim, Kyung-Ho, Cho, Seong-Jun, Kim, Byung-Oh, Pyo, Suhkneung
• Format: Article
• Language: English
• Subjects: Allicin; Apoptosis; Breast cancer; MAPK; Oestrogen receptor
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2016.06.019

•Allicin induced apoptosis in ERα+ and ERα− human breast cancer cells.•Allicin induced ROS-mediated apoptosis in MDA-MB-231 cells unlike in MCF7 cells.•Allicin induced both caspase-dependent and -independent apoptotic pathways.•ERα has a protective role during allicin-induced apoptosis in breast cancer cells. 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.