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Review
, 22 (1), 1-5

Anti-cancer Mechanism of Docosahexaenoic Acid in Pancreatic Carcinogenesis: A Mini-review

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Review

Anti-cancer Mechanism of Docosahexaenoic Acid in Pancreatic Carcinogenesis: A Mini-review

Mirae Park et al. J Cancer Prev.

Abstract

Pancreatic cancer is a highly aggressive malignant tumor of the digestive system and radical resection, which is available to very few patients, might be the only possibility for cure. Since therapeutic choices are limited at the advanced stage, prevention is more important for reducing incidence in high-risk individuals with family history of pancreatic cancer. Epidemiological studies have shown that a high consumption of fish oil or ω3-polyunsaturated fatty acids reduces the risk of pancreatic cancers. Dietary fish oil supplementation has shown to suppress pancreatic cancer development in animal models. Previous experimental studies revealed that several hallmarks of cancer involved in the pathogenesis of pancreatic cancer, such as the resistance to apoptosis, hyper-proliferation with abnormal Wnt/β-catenin signaling, expression of pro-angiogenic growth factors, and invasion. Docosahexaenoic acid (DHA) is a ω3-polyunsaturated fatty acid and rich in cold oceanic fish oil. DHA shows anti-cancer activity by inducing oxidative stress and apoptosis, inhibiting Wnt/β-catenin signaling, and decreasing extracellular matrix degradation and expression of pro-angiogenic factors in pancreatic cancer cells. This review will summarize anti-cancer mechanism of DHA in pancreatic carcinogenesis based on the recent studies.

Keywords: Anti-cancer effect; Docosahexaenoic acid; Pancreatic neoplasms.

Figures

Figure 1
Figure 1
The preventive effect of docosahexaenoic acid (DHA) against pancreatic cancer development. In pancreatic cancer cells, DHA induces glutathione (GSH) extrusion which increases the levels of reactive oxygen species (ROS) and caspase activation, resulting in ROS-mediated apoptosis. DHA also inhibits activation of Wnt/β-catenin signaling by increasing binding of glycogen synthase kinase-3β (GSK3β) to axin and reducing β-catenin accumulation as well as expression of cyclin E. Thus, DHA suppresses cancer cell proliferation. DHA down-regulates gran-zyme B, which degrades extracellular matrix (ECM) and promotes cancer cell invasion. DHA also reduces pro-angiogenic factors, such as VEGF and platelet-derived growth factor (PDGF). Therefore, DHA may inhibit resistance to cancer therapies and cancer development, and increase survival rate of pancreatic cancer patients.

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