AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis
Energy stress activates AMPK leading to metabolic plasticity and therapy resistance in cancer. Here, the authors show that AMPK activation decreases Prospero-related homeobox 1 (PROX1) levels impairing branched amino acid metabolism and tumourigenesis in liver and lung cancer models.
Main Authors: | , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2022-11-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-022-34747-y |
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author | Yanan Wang Mengjun Luo Fan Wang Yu Tong Linfeng Li Yu Shu Ke Qiao Lei Zhang Guoquan Yan Jing Liu Hongbin Ji Youhua Xie Yonglong Zhang Wei-Qiang Gao Yanfeng Liu |
author_facet | Yanan Wang Mengjun Luo Fan Wang Yu Tong Linfeng Li Yu Shu Ke Qiao Lei Zhang Guoquan Yan Jing Liu Hongbin Ji Youhua Xie Yonglong Zhang Wei-Qiang Gao Yanfeng Liu |
author_sort | Yanan Wang |
collection | DOAJ |
description | Energy stress activates AMPK leading to metabolic plasticity and therapy resistance in cancer. Here, the authors show that AMPK activation decreases Prospero-related homeobox 1 (PROX1) levels impairing branched amino acid metabolism and tumourigenesis in liver and lung cancer models. |
first_indexed | 2024-04-13T08:09:00Z |
format | Article |
id | doaj.art-6ee7698b436a40519f0b43a5be9fac7e |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-04-13T08:09:00Z |
publishDate | 2022-11-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-6ee7698b436a40519f0b43a5be9fac7e2022-12-22T02:55:03ZengNature PortfolioNature Communications2041-17232022-11-0113111810.1038/s41467-022-34747-yAMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesisYanan Wang0Mengjun Luo1Fan Wang2Yu Tong3Linfeng Li4Yu Shu5Ke Qiao6Lei Zhang7Guoquan Yan8Jing Liu9Hongbin Ji10Youhua Xie11Yonglong Zhang12Wei-Qiang Gao13Yanfeng Liu14Department of Laboratory Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong UniversityKey Laboratory of Medical Molecular Virology (MOE & MOH), Institute of Biomedical Sciences, Shanghai Medical College, Fudan UniversityState Key Laboratory of Oncogenes and Related Genes, Renji-Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong UniversityState Key Laboratory of Oncogenes and Related Genes, Renji-Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong UniversityState Key Laboratory of Oncogenes and Related Genes, Renji-Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong UniversityState Key Laboratory of Oncogenes and Related Genes, Renji-Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong UniversityKey Laboratory of Medical Molecular Virology (MOE & MOH), Institute of Biomedical Sciences, Shanghai Medical College, Fudan UniversityInstitute of Biomedical Sciences, Shanghai Medical College, Fudan UniversityInstitute of Biomedical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE & MOH), Institute of Biomedical Sciences, Shanghai Medical College, Fudan UniversityShanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesKey Laboratory of Medical Molecular Virology (MOE & MOH), Institute of Biomedical Sciences, Shanghai Medical College, Fudan UniversityCentral Laboratory, Shanghai Jiao Tong University Affiliated Sixth People’s HospitalState Key Laboratory of Oncogenes and Related Genes, Renji-Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong UniversityState Key Laboratory of Oncogenes and Related Genes, Renji-Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong UniversityEnergy stress activates AMPK leading to metabolic plasticity and therapy resistance in cancer. Here, the authors show that AMPK activation decreases Prospero-related homeobox 1 (PROX1) levels impairing branched amino acid metabolism and tumourigenesis in liver and lung cancer models.https://doi.org/10.1038/s41467-022-34747-y |
spellingShingle | Yanan Wang Mengjun Luo Fan Wang Yu Tong Linfeng Li Yu Shu Ke Qiao Lei Zhang Guoquan Yan Jing Liu Hongbin Ji Youhua Xie Yonglong Zhang Wei-Qiang Gao Yanfeng Liu AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis Nature Communications |
title | AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis |
title_full | AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis |
title_fullStr | AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis |
title_full_unstemmed | AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis |
title_short | AMPK induces degradation of the transcriptional repressor PROX1 impairing branched amino acid metabolism and tumourigenesis |
title_sort | ampk induces degradation of the transcriptional repressor prox1 impairing branched amino acid metabolism and tumourigenesis |
url | https://doi.org/10.1038/s41467-022-34747-y |
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