Abstract

BackgroundThere is limited evidence assessing the effects of omega-3 polyunsaturated fatty acids (PUFAs) on oesophageal adenocarcinoma, both in vitro and in vivo. We evaluated the effects of the omega-3 PUFA and oxaliplatin on OE33 and OE19 cells.MethodThe two oesophageal cells were treated with Omegaven® (fish oil emulsion), EPA, DHA and oxaliplatin and incubated for up to 144 h.ResultsThe following inhibitory effects were observed on OE33 cells: EPA reduced cell growth by 39% (p = 0.001), DHA by 59% (p < 0.000) and Oxaliplatin by 77% (p < 0.000). For OE19 cells, the EPA reduced growth by 1% (p = 0.992), DHA by 26% (p = 0.019) and oxaliplatin by 76% (p < 0.000). For both cells, Omegaven® resulted in reduced cell growth at intermediate concentrations (20-40 μM) and increased cell growth at low (10 μM) and high (50 μM) concentrations. DHA, Omegaven® and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein. DHA, Omegaven® and Oxaliplatin also led to significant downregulation of the total ERK1/2 and Akt proteins.ConclusionDHA, Omegaven® and oxaliplatin were associated with downregulation of p53 and VEGF in both cells. Of the PUFAs studied, DHA alone or in combination (Omegaven®) had greater in vitro anti-cancer effects than EPA alone.

Highlights

  • There is limited evidence assessing the effects of omega-3 polyunsaturated fatty acids (PUFAs) on oesophageal adenocarcinoma, both in vitro and in vivo

  • We evaluated the effect of the four single treatments (EPA, docosahexaenoic acid (DHA), Omegaven® and oxaliplatin) on OE33 and OE19 cell growth and expression of the following cytokines: IL-6, TNF-α and VEGF in the cell culture supernatant

  • The following inhibitory effects were observed on OE33 cells: Compared to control, eicosapentaenoic acid (EPA) reduced cell growth by 39% (p = 0.001), DHA reduced cell growth by 59% (p < 0.000) and Oxaliplatin reduced cell growth by 77% (p < 0.000)

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Summary

Introduction

There is limited evidence assessing the effects of omega-3 polyunsaturated fatty acids (PUFAs) on oesophageal adenocarcinoma, both in vitro and in vivo. A small amount of these PUFAs can be synthesized in the human body, approximately 2–10% of α-linolenic acid is converted to EPA and DHA. It is mainly dependent on external sources. Oesophagogastric cancer is considered to arise as a consequence of chronic inflammation [6]. This link is implicated for the development of gastric cancer as a result of Helicobacter pylori (H. pylori) related chronic gastritis and atrophy [7]. The link between inflammation and cancer is Eltweri et al Lipids in Health and Disease (2018) 17:19 strongest for adenocarcinoma as a result of chronic reflux associated inflammation [6]

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