Methyl jasmonate induced apoptosis in human prostate carcinoma cells via 5-Lipoxygenase dependent pathway
Daniel E. Ezekwudo, Robert C. Wang and J. Abiodun Elegbede
This work was supported in part by grants from the UNLV Planning Initiative Award and ACS #IRG-103719 (to JAE), UNLV (BRIN) Cytometry and Cancer Cores for equipment and instrumentation support. Methyl jasmonate – a plant stress hormone with striking resemblance to lipoxygenase products have been reported to induce apoptosis in several cancers. However, 5-HETE – a product of the lipoxygenase pathway has been implicated in human prostate cancer progression and yet possible interaction between methyl jasmonate and the lipoxygenase pathway has not been reported, thus, leaving some unanswered questions on the mechanism(s) of action by methyl jasmonate. Using cytotoxicity and flow cytometry assays (BrdU assay) as well as fluorescence microscopy, we investigated the effects of the methyl jasmonate on the proliferation of human prostate adenocarcinoma cell lines (DU-145, PC-3) in vitro and the potential interaction between methyl jasmonate and the lipoxygenase pathway. Methyl jasmonate (MJ) significantly (p= 0.01) inhibited the proliferation of human prostate carcinoma cells in dose- and kinetic-dependent manners and showed specific interaction with 5-lipoxygenase (5-LOX) enzyme pathway. Flow cytometric analyses and fluorescence microscopy confirmed that the inhibition of proliferation was via the induction of apoptosis. Based on our findings, it can be proposed that the interaction of methyl jasmonate with 5-lipoxygenase pathway may participate in the observed anticarcinogenic property.