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Biochim Biophys Acta Mol Cell Biol Lipids. 2020 Mar;1865(3):158579. doi: 10.1016/j.bbalip.2019.158579. Epub 2019 Nov 30.

Shotgun lipidomics-based characterization of the landscape of lipid metabolism in colorectal cancer.

Author information

1
Center for Regenerative Therapies Dresden, Technische Universität (TU) Dresden, Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
2
Department of Visceral Surgery, University Hospital Schleswig-Holstein, Christian-Albrechts-University Kiel, Kiel, Germany.
3
Neurosurgery, University Hospital Carl Gustav Carus, Technische Universität (TU) Dresden, Dresden, Germany.
4
Institute of Pathology, University Hospital Carl Gustav Carus, Technische Universität (TU) Dresden, Germany; National Center for Tumor Diseases (NCT), Partner Site Dresden, Dresden, Germany.
5
Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
6
Center for Regenerative Therapies Dresden, Technische Universität (TU) Dresden, Dresden, Germany; Department of Medicine I, University Hospital Carl Gustav Carus, Technische Universität (TU) Dresden, Dresden, Germany.
7
Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. Electronic address: shevchenko@mpi-cbg.de.
8
Center for Regenerative Therapies Dresden, Technische Universität (TU) Dresden, Dresden, Germany; Department of Medicine I, University Hospital Carl Gustav Carus, Technische Universität (TU) Dresden, Dresden, Germany. Electronic address: sebastian.zeissig@tu-dresden.de.

Abstract

Solid tumors are characterized by global metabolic alterations which contribute to their growth and progression. Altered gene expression profiles and plasma lipid composition suggested a role for metabolic reprogramming in colorectal cancer (CRC) development. However, a conclusive picture of CRC-associated lipidome alterations in the tumor tissue has not emerged. Here, we determined molar abundances of 342 species from 20 lipid classes in matched biopsies of CRC and adjacent normal mucosa. We demonstrate that in contrast to previous reports, CRC shows a largely preserved lipidome composition that resembles that of normal colonic mucosa. Important exceptions include increased levels of lyso-phosphatidylinositols in CRC and reduced abundance of ether phospholipids in advanced stages of CRC. As such, our observations challenge the concept of widespread alterations in lipid metabolism in CRC and rather suggest changes in the cellular lipid profile that are limited to selected lipids involved in signaling and the scavenging of reactive oxygen species.

KEYWORDS:

Cancer; Colon; Lipid metabolism; Mass spectrometry; Shotgun lipidomics

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