Lipid Metabolism in Cancer

A special issue of Metabolites (ISSN 2218-1989).

Deadline for manuscript submissions: closed (15 October 2021) | Viewed by 4403

Special Issue Editors


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Guest Editor
Centre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK
Interests: cancer metabolism; lipid metabolism; functional genomics; 3D models of cancer
Centre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK
Interests: cellular homeostasis and metabolism; cancer metabolism; lipid metabolism; mass spectrometry

Special Issue Information

Dear Colleagues,

Aberrant lipid metabolism has been identified in many human cancers and this raises the hope that the underlying metabolic enzymes may constitute novel and effective targets for cancer therapy. This Special Issue of Metabolites will focus on lipid metabolism in cancers and will include review and primary research articles on this topic. We invite the submission of manuscripts that tackle questions in biosynthesis, remodelling, uptake and oxidation of lipids, as well as lipid signalling, oxidative damage of lipids and lipid-protein interactions, both in cancer cells and other cell types within the tumour microenvironment. Many recent developments in the field of lipids and cancer have been enabled through the use of advanced technologies such as mass spectrometric profiling/measurement of lipids and high-content genetic and pharmacological screening. Therefore, manuscripts that address technological developments or perspectives in this area are also particularly welcomed. We hope to assemble a collection of interesting and thought-provoking articles that will inform future research directions and highlight the importance of lipid metabolism in cancers.

Dr. Barrie Peck 
Dr. Andy Finch
Guest Editors

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Keywords

  • lipids
  • metabolic pathways
  • biosynthesis
  • signalling
  • cancer therapy
  • mass spectrometry
  • lipidomics
  • high content screening

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Published Papers (1 paper)

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Research

20 pages, 9102 KiB  
Article
2-Hydroxypropyl-β-cyclodextrin Regulates the Epithelial to Mesenchymal Transition in Breast Cancer Cells by Modulating Cholesterol Homeostasis and Endoplasmic Reticulum Stress
by Yiyang Zhao, Linkang He, Tian Wang, Lifang Zhu and Nianlong Yan
Metabolites 2021, 11(8), 562; https://doi.org/10.3390/metabo11080562 - 23 Aug 2021
Cited by 10 | Viewed by 3614
Abstract
Cholesterol metabolism affects endoplasmic reticulum (ER) stress and modulates epithelial-mesenchymal transition (EMT). Our previous study demonstrated that 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) attenuated EMT by blocking the transforming growth factor (TGF)-β/Smad signaling pathway and activating ER stress in MDA-MB-231 cells. To further assess the detailed mechanisms [...] Read more.
Cholesterol metabolism affects endoplasmic reticulum (ER) stress and modulates epithelial-mesenchymal transition (EMT). Our previous study demonstrated that 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) attenuated EMT by blocking the transforming growth factor (TGF)-β/Smad signaling pathway and activating ER stress in MDA-MB-231 cells. To further assess the detailed mechanisms between cholesterol metabolism, ER stress, and EMT, LXR-623 (an agonist of LXRα) and simvastatin were used to increase and decrease cholesterol efflux and synthesis, respectively. Here, we found that high HP-β-CD concentrations could locally increase cholesterol levels in the ER by decreasing LXRα expression and increasing Hydroxymethylglutaryl-Coenzyme A reductase (HMGCR) expression in MDA-MB-231 and BT-549 cells, which triggered ER stress and inhibited EMT. Meanwhile, tunicamycin-induced ER stress blocked the TGF-β/Smad signaling pathway. However, low HP-β-CD concentrations can decrease the level of membrane cholesterol, enhance the TGF-β receptor I levels in lipid rafts, which helped to activate TGF-β/Smad signaling pathway, inhibit ER stress and elevate EMT. Based on our findings, the use of high HP-β-CD concentration can lead to cholesterol accumulation in the ER, thereby inducing ER stress, which directly suppresses TGF-β pathway-induced EMT. However, HP-β-CD is proposed to deplete membrane cholesterol at low concentrations and concurrently inhibit ER stress and induce EMT by promoting the TGF-β signaling pathways. Full article
(This article belongs to the Special Issue Lipid Metabolism in Cancer)
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