12-Lipoxygenase inhibition induced apoptosis in human gastric cancer cells

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Abstract

Arachidonic acid release from membrane phospholipids is essential for tumour cell proliferation. Lipoxygenases constitute a pathway for arachidonate metabolism. The present study investigated the expression of 12-lipoxygenase and its effect on cell proliferation as well as survival in two human gastric cancer cell lines (AGS and MKN-28). RT-PCR and western blots, respectively, showed 12-LOX mRNA and protein expression in both AGS and MKN-28 cell lines. Treatment with a 12-LOX inhibitor, baicalein, significantly inhibited cancer cell proliferation, but a metabolite of 12-LOX activity, 12 hydroxyeicosatetraenoic acid (12-HETE) reversed baicalein-induced growth inhibition. Furthermore, the blockade of the 12-LOX pathway through a 12-LOX inhibitor and antisense induced apoptosis of gastric cancer cell lines. The biochemical characteristics of apoptosis were p53-independent combined with a decrease in bcl-2 expression. Caspase-7 was proteolytically activated and responsible for the apoptosis execution.

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Wong, B. C. Y., Wang, W. P., Cho, C. H., Fan, X. M., Lin, M. C. M., Kung, H. F., & Lam, S. K. (2001). 12-Lipoxygenase inhibition induced apoptosis in human gastric cancer cells. Carcinogenesis, 22(9), 1349–1354. https://doi.org/10.1093/carcin/22.9.1349

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