Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells

Metastasizing cancer cells rewire their metabolism to support their malignant phenotypes. Here, the authors show that the acquisition of a metastatic phenotype in breast cancer cell lines results in increased proline catabolism and that inhibition of this pathway decreases lung metastasis formation...

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Main Authors: Ilaria Elia, Dorien Broekaert, Stefan Christen, Ruben Boon, Enrico Radaelli, Martin F. Orth, Catherine Verfaillie, Thomas G. P. Grünewald, Sarah-Maria Fendt
Format: Article
Language:English
Published: Nature Publishing Group 2017-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms15267
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spelling doaj-69af72ab34f4448d9adc1e35ac453ca92021-05-11T07:18:41ZengNature Publishing GroupNature Communications2041-17232017-05-018111110.1038/ncomms15267Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cellsIlaria Elia0Dorien Broekaert1Stefan Christen2Ruben Boon3Enrico Radaelli4Martin F. Orth5Catherine Verfaillie6Thomas G. P. Grünewald7Sarah-Maria Fendt8Laboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer BiologyLaboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer BiologyLaboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer BiologyStem Cell Institute, KU LeuvenCenter for the Biology of Disease, VIB Leuven and Center for Human Genetics, KU LeuvenMax-Eder Research Group for Pediatric Sarcoma Biology, Institute of PathologyStem Cell Institute, KU LeuvenMax-Eder Research Group for Pediatric Sarcoma Biology, Institute of PathologyLaboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer BiologyMetastasizing cancer cells rewire their metabolism to support their malignant phenotypes. Here, the authors show that the acquisition of a metastatic phenotype in breast cancer cell lines results in increased proline catabolism and that inhibition of this pathway decreases lung metastasis formation in two mouse models.https://doi.org/10.1038/ncomms15267
collection DOAJ
language English
format Article
sources DOAJ
author Ilaria Elia
Dorien Broekaert
Stefan Christen
Ruben Boon
Enrico Radaelli
Martin F. Orth
Catherine Verfaillie
Thomas G. P. Grünewald
Sarah-Maria Fendt
spellingShingle Ilaria Elia
Dorien Broekaert
Stefan Christen
Ruben Boon
Enrico Radaelli
Martin F. Orth
Catherine Verfaillie
Thomas G. P. Grünewald
Sarah-Maria Fendt
Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
Nature Communications
author_facet Ilaria Elia
Dorien Broekaert
Stefan Christen
Ruben Boon
Enrico Radaelli
Martin F. Orth
Catherine Verfaillie
Thomas G. P. Grünewald
Sarah-Maria Fendt
author_sort Ilaria Elia
title Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
title_short Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
title_full Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
title_fullStr Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
title_full_unstemmed Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
title_sort proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2017-05-01
description Metastasizing cancer cells rewire their metabolism to support their malignant phenotypes. Here, the authors show that the acquisition of a metastatic phenotype in breast cancer cell lines results in increased proline catabolism and that inhibition of this pathway decreases lung metastasis formation in two mouse models.
url https://doi.org/10.1038/ncomms15267
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