Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation

Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation

Cancer cells must develop distinct metabolic adaptations to survive in challenging metastatic environments. Here, the authors find, via an in vivo RNAi screen, that the aldo-keto reductase AKR1B10 limits the toxic side effects of oxidative stress to sustain fatty acid oxidation and promote metastati...

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Main Authors: Antoinette van Weverwijk, Nikolaos Koundouros, Marjan Iravani, Matthew Ashenden, Qiong Gao, George Poulogiannis, Ute Jungwirth, Clare M. Isacke
Format: Article
Language:English
Published: Nature Publishing Group 2019-06-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-019-10592-4
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spelling doaj-58bc19073e294af1870da5b4ec93e4312021-05-11T11:49:03ZengNature Publishing GroupNature Communications2041-17232019-06-0110111310.1038/s41467-019-10592-4Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidationAntoinette van Weverwijk0Nikolaos Koundouros1Marjan Iravani2Matthew Ashenden3Qiong Gao4George Poulogiannis5Ute Jungwirth6Clare M. Isacke7The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer ResearchDepartment of Cancer Biology, The Institute of Cancer ResearchThe Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer ResearchThe Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer ResearchThe Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer ResearchDepartment of Cancer Biology, The Institute of Cancer ResearchThe Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer ResearchThe Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer ResearchCancer cells must develop distinct metabolic adaptations to survive in challenging metastatic environments. Here, the authors find, via an in vivo RNAi screen, that the aldo-keto reductase AKR1B10 limits the toxic side effects of oxidative stress to sustain fatty acid oxidation and promote metastatic colonisation.https://doi.org/10.1038/s41467-019-10592-4
collection DOAJ
language English
format Article
sources DOAJ
author Antoinette van Weverwijk
Nikolaos Koundouros
Marjan Iravani
Matthew Ashenden
Qiong Gao
George Poulogiannis
Ute Jungwirth
Clare M. Isacke
spellingShingle Antoinette van Weverwijk
Nikolaos Koundouros
Marjan Iravani
Matthew Ashenden
Qiong Gao
George Poulogiannis
Ute Jungwirth
Clare M. Isacke
Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation
Nature Communications
author_facet Antoinette van Weverwijk
Nikolaos Koundouros
Marjan Iravani
Matthew Ashenden
Qiong Gao
George Poulogiannis
Ute Jungwirth
Clare M. Isacke
author_sort Antoinette van Weverwijk
title Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation
title_short Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation
title_full Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation
title_fullStr Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation
title_full_unstemmed Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation
title_sort metabolic adaptability in metastatic breast cancer by akr1b10-dependent balancing of glycolysis and fatty acid oxidation
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2019-06-01
description Cancer cells must develop distinct metabolic adaptations to survive in challenging metastatic environments. Here, the authors find, via an in vivo RNAi screen, that the aldo-keto reductase AKR1B10 limits the toxic side effects of oxidative stress to sustain fatty acid oxidation and promote metastatic colonisation.
url https://doi.org/10.1038/s41467-019-10592-4
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