Role of JNK Activation and Mitochondrial Bax Translocation in Allicin-Induced Apoptosis in Human Ovarian Cancer SKOV3 Cells

Abstract EN

Allicin, the major component of freshly crushed garlic, is one of the most biologically active compounds of garlic; it has been reported to induce apoptosis in cancer cells; however, the mechanism by which allicin exerts its apoptotic effects is not fully understood.

The aim of the present study was to further elucidate the apoptotic pathways induced by allicin in the human ovarian cancer cell line SKOV3.

Methods.

Cell proliferation and apoptosis were measured by cell-counting assay and flow cytometry analysis.

Activation of the signaling pathway was screened by human phospho-kinase array analysis, and the activated pathway and its related proteins were further confirmed by western blot analysis.

Results.

Allicin induced SKOV3 cell apoptosis and JNK phosphorylation in a time- and dose-dependent manner, but these were significantly blocked by SP600125 (an inhibitor of JNK).

The findings suggest that JNK phosphorylation is related to the action of allicin on SKOV3 cells.

Furthermore, JNK activation induced Bcl-2 family activation, triggered mitochondria-mediated signaling pathways, and led to the translocation of a considerable amount of Bax and cytochrome c release.

Conclusions.

JNK activation and mitochondrial Bax translocation are involved in allicin-induced apoptosis in SKOV3 cells.

Our data input new insights to the literature of allicin-induced apoptosis.