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Lipid metabolic reprogramming in cancer cells

Many human diseases, including metabolic, immune and central nervous system disorders, as well as cancer, are the consequence of an alteration in lipid metabolic enzymes and their pathways. This illustrates the fundamental role played by lipids in maintaining membrane homeostasis and normal function...

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Detalles Bibliográficos
Autores principales: Beloribi-Djefaflia, S, Vasseur, S, Guillaumond, F
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728678/
https://www.ncbi.nlm.nih.gov/pubmed/26807644
http://dx.doi.org/10.1038/oncsis.2015.49
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author Beloribi-Djefaflia, S
Vasseur, S
Guillaumond, F
author_facet Beloribi-Djefaflia, S
Vasseur, S
Guillaumond, F
author_sort Beloribi-Djefaflia, S
collection PubMed
description Many human diseases, including metabolic, immune and central nervous system disorders, as well as cancer, are the consequence of an alteration in lipid metabolic enzymes and their pathways. This illustrates the fundamental role played by lipids in maintaining membrane homeostasis and normal function in healthy cells. We reviewed the major lipid dysfunctions occurring during tumor development, as determined using systems biology approaches. In it, we provide detailed insight into the essential roles exerted by specific lipids in mediating intracellular oncogenic signaling, endoplasmic reticulum stress and bidirectional crosstalk between cells of the tumor microenvironment and cancer cells. Finally, we summarize the advances in ongoing research aimed at exploiting the dependency of cancer cells on lipids to abolish tumor progression.
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spelling pubmed-47286782016-02-08 Lipid metabolic reprogramming in cancer cells Beloribi-Djefaflia, S Vasseur, S Guillaumond, F Oncogenesis Review Many human diseases, including metabolic, immune and central nervous system disorders, as well as cancer, are the consequence of an alteration in lipid metabolic enzymes and their pathways. This illustrates the fundamental role played by lipids in maintaining membrane homeostasis and normal function in healthy cells. We reviewed the major lipid dysfunctions occurring during tumor development, as determined using systems biology approaches. In it, we provide detailed insight into the essential roles exerted by specific lipids in mediating intracellular oncogenic signaling, endoplasmic reticulum stress and bidirectional crosstalk between cells of the tumor microenvironment and cancer cells. Finally, we summarize the advances in ongoing research aimed at exploiting the dependency of cancer cells on lipids to abolish tumor progression. Nature Publishing Group 2016-01 2016-01-25 /pmc/articles/PMC4728678/ /pubmed/26807644 http://dx.doi.org/10.1038/oncsis.2015.49 Text en Copyright © 2016 Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Review
Beloribi-Djefaflia, S
Vasseur, S
Guillaumond, F
Lipid metabolic reprogramming in cancer cells
title Lipid metabolic reprogramming in cancer cells
title_full Lipid metabolic reprogramming in cancer cells
title_fullStr Lipid metabolic reprogramming in cancer cells
title_full_unstemmed Lipid metabolic reprogramming in cancer cells
title_short Lipid metabolic reprogramming in cancer cells
title_sort lipid metabolic reprogramming in cancer cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728678/
https://www.ncbi.nlm.nih.gov/pubmed/26807644
http://dx.doi.org/10.1038/oncsis.2015.49
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