Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia

Cancer cells under stress use acetate to maintain the acetyl-CoA pool and fuel lipid biosynthesis. Here, the authors show that acetate also promotes de novo lipid synthesis by increasing histone acetylation at the promoters of lipogenic enzymes ACACA and FASN, thus inducing their expression.

Bibliographic Details
Main Authors: Xue Gao, Shu-Hai Lin, Feng Ren, Jin-Tao Li, Jia-Jia Chen, Chuan-Bo Yao, Hong-Bin Yang, Shu-Xia Jiang, Guo-Quan Yan, Di Wang, Yi Wang, Ying Liu, Zongwei Cai, Ying-Ying Xu, Jing Chen, Wenqiang Yu, Peng-Yuan Yang, Qun-Ying Lei
Format: Article
Language:English
Published: Nature Portfolio 2016-06-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms11960
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author Xue Gao
Shu-Hai Lin
Feng Ren
Jin-Tao Li
Jia-Jia Chen
Chuan-Bo Yao
Hong-Bin Yang
Shu-Xia Jiang
Guo-Quan Yan
Di Wang
Yi Wang
Ying Liu
Zongwei Cai
Ying-Ying Xu
Jing Chen
Wenqiang Yu
Peng-Yuan Yang
Qun-Ying Lei
author_facet Xue Gao
Shu-Hai Lin
Feng Ren
Jin-Tao Li
Jia-Jia Chen
Chuan-Bo Yao
Hong-Bin Yang
Shu-Xia Jiang
Guo-Quan Yan
Di Wang
Yi Wang
Ying Liu
Zongwei Cai
Ying-Ying Xu
Jing Chen
Wenqiang Yu
Peng-Yuan Yang
Qun-Ying Lei
author_sort Xue Gao
collection DOAJ
description Cancer cells under stress use acetate to maintain the acetyl-CoA pool and fuel lipid biosynthesis. Here, the authors show that acetate also promotes de novo lipid synthesis by increasing histone acetylation at the promoters of lipogenic enzymes ACACA and FASN, thus inducing their expression.
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spelling doaj.art-b8194c2aa98945ec80fb6bb93952191d2022-12-21T19:27:23ZengNature PortfolioNature Communications2041-17232016-06-017111410.1038/ncomms11960Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxiaXue Gao0Shu-Hai Lin1Feng Ren2Jin-Tao Li3Jia-Jia Chen4Chuan-Bo Yao5Hong-Bin Yang6Shu-Xia Jiang7Guo-Quan Yan8Di Wang9Yi Wang10Ying Liu11Zongwei Cai12Ying-Ying Xu13Jing Chen14Wenqiang Yu15Peng-Yuan Yang16Qun-Ying Lei17and Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan UniversityDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine (SJTU-SM)and Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan UniversityDepartment of Chemistry, State Key Laboratory of Environmental and Biological Analysis, Hong Kong Baptist Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan UniversityDepartment of Pathology, School of Basic Medical Sciences, Fudan UniversityDepartment of Chemistry, State Key Laboratory of Environmental and Biological Analysis, Hong Kong Baptist Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan UniversityDepartment of Hematology and Medical Oncology, Winship Cancer Institute of Emory, Emory University School of Medicineand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan Universityand Department of Biochemistry and Molecular Biology, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, School of Basic Medical Sciences, and Institutes of Biomedical Sciences, Fudan UniversityCancer cells under stress use acetate to maintain the acetyl-CoA pool and fuel lipid biosynthesis. Here, the authors show that acetate also promotes de novo lipid synthesis by increasing histone acetylation at the promoters of lipogenic enzymes ACACA and FASN, thus inducing their expression.https://doi.org/10.1038/ncomms11960
spellingShingle Xue Gao
Shu-Hai Lin
Feng Ren
Jin-Tao Li
Jia-Jia Chen
Chuan-Bo Yao
Hong-Bin Yang
Shu-Xia Jiang
Guo-Quan Yan
Di Wang
Yi Wang
Ying Liu
Zongwei Cai
Ying-Ying Xu
Jing Chen
Wenqiang Yu
Peng-Yuan Yang
Qun-Ying Lei
Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
Nature Communications
title Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
title_full Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
title_fullStr Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
title_full_unstemmed Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
title_short Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
title_sort acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
url https://doi.org/10.1038/ncomms11960
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