EPA, an omega-3 fatty acid, induces apoptosis in human pancreatic cancer cells: role of ROS accumulation, caspase-8 activation, and autophagy induction
- EPA, an omega-3 fatty acid, induces apoptosis in human pancreatic cancer cells: role of ROS accumulation, caspase-8 activation, and autophagy induction
- Fukui Masayuki; 강기성; K. Okada; Bao Ting Zhu
- EPA; Apoptosis; Pancreatic cancer; ROS; EICOSAPENTAENOIC ACID; DOCOSAHEXAENOIC ACID; OMEGA-3 POLYUNSATURATED FATTY ACIDS; AUTOPHAGY
- Issue Date
- Journal of cellular biochemistry
- VOL 114, NO 1, 192-203
- In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause
ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al. , PLoS ONE 5:
e10296). In this study, we showed that the pancreas has a unique ability to accumulate EPA at a level markedly higher than several other
tissues analyzed. Based on this finding, we sought to further investigate the anticancer actions of EPA and its analog DHA in human pancreatic
cancer cells using both in vitro and in vivo models. EPA and DHA were found to induce ROS accumulation and caspase-8-dependent cell death
in human pancreatic cancer cells (MIA-PaCa-2 and Capan-2) in vitro. Feeding animals with a diet supplemented with 5% fish oil, which
contains high levels of EPA and DHA, also strongly suppresses the growth of MIA-PaCa-2 human pancreatic cancer xenografts in athymic
nude mice, by inducing oxidative stress and cell death. In addition, we showed that EPA can concomitantly induce autophagy in these cancer
cells, and the induction of autophagy diminishes its ability to induce apoptotic cell death. It is therefore suggested that combination of EPA
with an autophagy inhibitor may be a useful strategy in increasing the therapeutic effectiveness in pancreatic cancer.
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