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. 2019 Dec 10;122(1):4–22. doi: 10.1038/s41416-019-0650-z

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Fatty acids (FAs) regulate membrane architecture and oncogenic signalling pathways. a Membrane fluidity is largely determined by cholesterol levels and degree of FA desaturation. Cancer cells displaying elevated de novo lipogenesis can synthesise saturated phospholipids, which not only increases membrane rigidity, but also protects against peroxidation induced by reactive oxygen species. Conversely, highly migratory cells display more fluid membranes as a result of increased desaturation and cholesterol abundance, thus contributing to the epithelial-to-mesenchymal transition and metastasis. b FAs and their synthetic products also function as secondary messengers in signalling pathways, with the best characterised being the phosphoinositides. PI(3,4,5)P₃ activates oncogenic AKT, and contributes to hyperactivation of mTORC1 and mTORC2. In addition, PI(3)P stimulates SGK3 that promotes tumorigenesis independently of AKT. Finally, phosphatidic acid can also directly bind to and activate the mTOR complexes. Abbreviations: PI3Kα, phosphoinositide 3-kinase α; PI(4,5)P₂, phosphatidylinositol (4,5)-bisphosphate; PI(3,4,5)P₃, phosphatidylinositol (3,4,5)-trisphosphate; PI(3,4)P₂, phosphatidylinositol (3,4)-bisphosphate; PI(3)P, phosphatidylinositol 3-phosphate; mTORC, mammalian target of rapamycin complex; PA, phosphatidic acid; PTEN, phosphatase and tensin homologue; SGK3, serum- and glucocorticoid-induced protein kinase-3; INPP4B, inositol polyphosphate-4-phosphatase type II B.