Differential apoptotic response of human breast cancer cells to allicin

Allicin induces apoptosis in various carcinoma cells and inhibits tumorigenesis. However, the precise mechanism of allicin‐induced apoptosis is still unclear in human breast cancer cells. We investigated the effect of allicin on cell proliferation, apoptosis, and its pathway in the estrogen receptor (ER)‐positive MCF‐7 and ER‐negative MDA‐MB‐231 human breast cancer cells. The results showed that allicin decreased concentration‐dependently cell proliferation in MDA‐MB‐231 cells. Moreover, allicin induced the mitochondrial/caspase apoptotic pathway caused by a decrease in mitochondrial membrane potential due to the up‐regulation of Bax and the down‐regulation of Bcl2 and Bcl‐xL. In contrast, MCF‐7 cells were insensitive to allicin‐induced apoptosis. However, treatment with a combination of allicin and ER antagonist resulted in a decrease in proliferation and induced apoptosis as compared with single treatment. The results indicate that ER expression may be important for apoptosis regulation in allicin‐treated MCF‐7 cells. In both cells, allicin activated ERK1/2, p38 and JNK in a concentration‐ and time‐dependent manner. In addition, allicin‐induced cell death was reversed by specific inhibitors of p38 and JNK in MDA‐MB‐231, but not in MCF‐7 cells. Taken together, the data suggest that allicin inhibits cell growth and induces apoptosis through MAPKs and ER signaling pathways in MDA‐MB‐231 cells.