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Polyunsaturated fatty acid biosynthesis pathway determines ferroptosis sensitivity in gastric cancer
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Polyunsaturated fatty acid biosynthesis pathway determines ferroptosis sensitivity in gastric cancer
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Polyunsaturated fatty acid biosynthesis pathway determines ferroptosis sensitivity in gastric cancer
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Journal Article
Polyunsaturated fatty acid biosynthesis pathway determines ferroptosis sensitivity in gastric cancer
2020
Overview
Ferroptosis is an iron-dependent regulated necrosis mediated by lipid peroxidation. Cancer cells survive under metabolic stress conditions by altering lipid metabolism, which may alter their sensitivity to ferroptosis. However, the association between lipid metabolism and ferroptosis is not completely understood. In this study, we found that the expression of elongation of very longchain fatty acid protein 5 (ELOVL5) and fatty acid desaturase 1 (FADS1) is up-regulated in mesenchymal-type gastric cancer cells (GCs), leading to ferroptosis sensitization. In contrast, these enzymes are silenced by DNA methylation in intestinal-type GCs, rendering cells resistant to ferroptosis. Lipid profiling and isotope tracing analyses revealed that intestinal-type GCs are unable to generate arachidonic acid (AA) and adrenic acid (AdA) from linoleic acid. AA supplementation of intestinal-type GCs restores their sensitivity to ferroptosis. Based on these data, the polyunsaturated fatty acid (PUFA) biosynthesis pathway plays an essential role in ferroptosis; thus, this pathway potentially represents a marker for predicting the efficacy of ferroptosis-mediated cancer therapy.
Publisher
National Academy of Sciences
Subject
/ Arachidonic Acid - metabolism
/ Arachidonic Acid - pharmacology
/ Cancer
/ Fatty Acid Desaturases - genetics
/ Fatty Acid Desaturases - metabolism
/ Fatty Acid Elongases - genetics
/ Fatty Acid Elongases - metabolism
/ Fatty Acids, Unsaturated - biosynthesis
/ Fatty Acids, Unsaturated - genetics
/ Fatty Acids, Unsaturated - metabolism
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Lipids
/ Necrosis
/ Stomach Neoplasms - drug therapy
/ Stomach Neoplasms - genetics
/ Stomach Neoplasms - metabolism
