OBJECTIVES: Clinical studies have shown that administration of eicosapentaenoic acid (EPA) to patients who have unresectable pancreatic cancer induces marked attenuation of cachexia. However, the exact mechanisms of the beneficial effect of EPA on pancreatic cancer are unknown. This examined the effect of EPA on proliferation of human pancreatic cancer cell lines and sought to clarify its mechanisms. METHODS: The effects of EPA on proliferation of three human pancreatic cancer cell lines (SW1990, AsPC-1, and PANC-1) were assessed. Induction of apoptosis and expressions of apoptosis-related proteins were measured. The effect of EPA on cyclo-oxygenase-2 expression in these cell lines was determined. RESULTS: EPA inhibited proliferation of all three human pancreatic cancer cell lines in a dose-dependent fashion. Simultaneously, EPA treatment induced apoptosis and this was associated with caspase-3 activation. EPA treatment was also associated with a decrease in intracellular levels of cyclo-oxygenase-2 protein. CONCLUSION: We have demonstrated that EPA inhibits human pancreatic cancer cell growth due at least in part to the induction of apoptotic cell death. Such apoptosis is associated with activation of caspase-3 and suppression of cyclo-oxygenase-2 expression. Greater understanding of the molecular events associated with the biological activity of EPA should enhance the therapeutic potential of administration of EPA to patients who have pancreatic cancer.
OBJECTIVES: Clinical studies have shown that administration of eicosapentaenoic acid (EPA) to patients who have unresectable pancreatic cancer induces marked attenuation of cachexia. However, the exact mechanisms of the beneficial effect of EPA on pancreatic cancer are unknown. This examined the effect of EPA on proliferation of humanpancreatic cancer cell lines and sought to clarify its mechanisms. METHODS: The effects of EPA on proliferation of three humanpancreatic cancer cell lines (SW1990, AsPC-1, and PANC-1) were assessed. Induction of apoptosis and expressions of apoptosis-related proteins were measured. The effect of EPA on cyclo-oxygenase-2 expression in these cell lines was determined. RESULTS:EPA inhibited proliferation of all three humanpancreatic cancer cell lines in a dose-dependent fashion. Simultaneously, EPA treatment induced apoptosis and this was associated with caspase-3 activation. EPA treatment was also associated with a decrease in intracellular levels of cyclo-oxygenase-2 protein. CONCLUSION: We have demonstrated that EPA inhibits humanpancreatic cancer cell growth due at least in part to the induction of apoptotic cell death. Such apoptosis is associated with activation of caspase-3 and suppression of cyclo-oxygenase-2 expression. Greater understanding of the molecular events associated with the biological activity of EPA should enhance the therapeutic potential of administration of EPA to patients who have pancreatic cancer.
Authors: Antonio Casado-Díaz; Carlos Ferreiro-Vera; Feliciano Priego-Capote; Gabriel Dorado; María Dolores Luque-de-Castro; José Manuel Quesada-Gómez Journal: Genes Nutr Date: 2013-12-14 Impact factor: 5.523
Authors: Matthew J Strouch; Yongzeng Ding; Mohammad R Salabat; Laleh G Melstrom; Kevin Adrian; Christopher Quinn; Carolyn Pelham; Sambasiva Rao; Thomas E Adrian; David J Bentrem; Paul J Grippo Journal: J Surg Res Date: 2009-05-15 Impact factor: 2.192
Authors: Xiaoyu Yang; Yi Xu; Amanda Brooks; Bin Guo; Keith W Miskimins; Steven Y Qian Journal: Free Radic Biol Med Date: 2016-06-28 Impact factor: 7.376
Authors: Yongzeng Ding; Bhargava Mullapudi; Carolina Torres; Emman Mascariñas; Georgina Mancinelli; Andrew M Diaz; Ronald McKinney; Morgan Barron; Michelle Schultz; Michael Heiferman; Mireille Wojtanek; Kevin Adrian; Brian DeCant; Sambasiva Rao; Michel Ouellette; Ming-Sound Tsao; David J Bentrem; Paul J Grippo Journal: Nutrients Date: 2018-09-12 Impact factor: 5.717