Bromodomain-containing protein 4 (BRD4) as an epigenetic regulator of fatty acid metabolism genes and ferroptosis

Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid metabolism and ferroptosis remain largely unknown. Results from the drug screening of 464 inhibitors (for 164 targets) applied to ferroptosis cel...

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Published inCell death & disease Vol. 13; no. 10; pp. 912 - 17
Main Authors Yang, Minghua, Liu, Ke, Chen, Pan, Zhu, Hongyi, Wang, Junjie, Huang, Jun
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 29.10.2022
Springer Nature B.V
Nature Publishing Group
Subjects
631/337/176/2016
631/337/2265
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Drug screening
Enhancers
Epigenesis, Genetic
Epigenetics
Fatty Acids
Ferroptosis
Ferroptosis - genetics
Immunology
Life Sciences
Lipid metabolism
Lipid Metabolism - genetics
Lipids
Metabolism
Mitochondria
Molecular modelling
Nuclear Proteins - metabolism
Oxidation
Polyunsaturated fatty acids
Transcription Factors - metabolism
Online AccessGet full text
ISSN2041-4889
2041-4889
DOI10.1038/s41419-022-05344-0

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Abstract Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid metabolism and ferroptosis remain largely unknown. Results from the drug screening of 464 inhibitors (for 164 targets) applied to ferroptosis cells indicated that 4 inhibitors targeted bromodomain-containing protein 4 (BRD4) significantly inhibiting erastin-induced ferroptosis. Functional studies proved that the loss of BRD4 weakened oxidative catabolism in mitochondria, protecting cells from the excessive accumulation of lipid peroxides. Mechanism research revealed that the transcriptional levels of fatty acid metabolism-related genes (HADH, ACSL1 and ACAA2) participating in the β-oxidation of fatty acids (FAO) and polyunsaturated fatty acids (PUFAs) synthesis depended on the activity of super-enhancers (SEs) formed by BRD4 and HMGB2 in their promoter regions. Conclusively, this study demonstrated that BRD4 was indispensable for fatty acid metabolism based on its epigenetic regulatory mechanisms and affecting erastin-induced ferroptosis, providing a new theoretical reference for understanding the relationship between lipid metabolism and ferroptosis deeply.
AbstractList Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid metabolism and ferroptosis remain largely unknown. Results from the drug screening of 464 inhibitors (for 164 targets) applied to ferroptosis cells indicated that 4 inhibitors targeted bromodomain-containing protein 4 (BRD4) significantly inhibiting erastin-induced ferroptosis. Functional studies proved that the loss of BRD4 weakened oxidative catabolism in mitochondria, protecting cells from the excessive accumulation of lipid peroxides. Mechanism research revealed that the transcriptional levels of fatty acid metabolism-related genes (HADH, ACSL1 and ACAA2) participating in the β-oxidation of fatty acids (FAO) and polyunsaturated fatty acids (PUFAs) synthesis depended on the activity of super-enhancers (SEs) formed by BRD4 and HMGB2 in their promoter regions. Conclusively, this study demonstrated that BRD4 was indispensable for fatty acid metabolism based on its epigenetic regulatory mechanisms and affecting erastin-induced ferroptosis, providing a new theoretical reference for understanding the relationship between lipid metabolism and ferroptosis deeply.Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid metabolism and ferroptosis remain largely unknown. Results from the drug screening of 464 inhibitors (for 164 targets) applied to ferroptosis cells indicated that 4 inhibitors targeted bromodomain-containing protein 4 (BRD4) significantly inhibiting erastin-induced ferroptosis. Functional studies proved that the loss of BRD4 weakened oxidative catabolism in mitochondria, protecting cells from the excessive accumulation of lipid peroxides. Mechanism research revealed that the transcriptional levels of fatty acid metabolism-related genes (HADH, ACSL1 and ACAA2) participating in the β-oxidation of fatty acids (FAO) and polyunsaturated fatty acids (PUFAs) synthesis depended on the activity of super-enhancers (SEs) formed by BRD4 and HMGB2 in their promoter regions. Conclusively, this study demonstrated that BRD4 was indispensable for fatty acid metabolism based on its epigenetic regulatory mechanisms and affecting erastin-induced ferroptosis, providing a new theoretical reference for understanding the relationship between lipid metabolism and ferroptosis deeply.
Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid metabolism and ferroptosis remain largely unknown. Results from the drug screening of 464 inhibitors (for 164 targets) applied to ferroptosis cells indicated that 4 inhibitors targeted bromodomain-containing protein 4 (BRD4) significantly inhibiting erastin-induced ferroptosis. Functional studies proved that the loss of BRD4 weakened oxidative catabolism in mitochondria, protecting cells from the excessive accumulation of lipid peroxides. Mechanism research revealed that the transcriptional levels of fatty acid metabolism-related genes (HADH, ACSL1 and ACAA2) participating in the β-oxidation of fatty acids (FAO) and polyunsaturated fatty acids (PUFAs) synthesis depended on the activity of super-enhancers (SEs) formed by BRD4 and HMGB2 in their promoter regions. Conclusively, this study demonstrated that BRD4 was indispensable for fatty acid metabolism based on its epigenetic regulatory mechanisms and affecting erastin-induced ferroptosis, providing a new theoretical reference for understanding the relationship between lipid metabolism and ferroptosis deeply.
Abstract Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid metabolism and ferroptosis remain largely unknown. Results from the drug screening of 464 inhibitors (for 164 targets) applied to ferroptosis cells indicated that 4 inhibitors targeted bromodomain-containing protein 4 (BRD4) significantly inhibiting erastin-induced ferroptosis. Functional studies proved that the loss of BRD4 weakened oxidative catabolism in mitochondria, protecting cells from the excessive accumulation of lipid peroxides. Mechanism research revealed that the transcriptional levels of fatty acid metabolism-related genes (HADH, ACSL1 and ACAA2) participating in the β-oxidation of fatty acids (FAO) and polyunsaturated fatty acids (PUFAs) synthesis depended on the activity of super-enhancers (SEs) formed by BRD4 and HMGB2 in their promoter regions. Conclusively, this study demonstrated that BRD4 was indispensable for fatty acid metabolism based on its epigenetic regulatory mechanisms and affecting erastin-induced ferroptosis, providing a new theoretical reference for understanding the relationship between lipid metabolism and ferroptosis deeply.
ArticleNumber 912
Author Zhu, Hongyi
Yang, Minghua
Chen, Pan
Liu, Ke
Wang, Junjie
Huang, Jun
Author_xml – sequence: 1
  givenname: Minghua
  surname: Yang
  fullname: Yang, Minghua
  organization: Department of Pediatrics, The Third Xiangya Hospital, Central South University
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  organization: Department of Ophthalmology, The Second Xiangya Hospital, Central South University
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  fullname: Chen, Pan
  organization: Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University
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  givenname: Hongyi
  surname: Zhu
  fullname: Zhu, Hongyi
  organization: Department of Gastroenterology, The Second Xiangya Hospital, Central South University
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  givenname: Junjie
  surname: Wang
  fullname: Wang, Junjie
  organization: Department of Orthopedics, The Second Xiangya Hospital, Central South University
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  orcidid: 0000-0002-4798-6191
  surname: Huang
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  email: 505447@csu.edu.cn
  organization: Department of Orthopedics, The Second Xiangya Hospital, Central South University
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SSID ssj0000330256
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Snippet Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between lipid...
Abstract Reprogramming lipid metabolism is considered a fundamental step in tumourigenesis that influences ferroptosis. However, molecular mechanisms between...
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pubmedcentral
proquest
pubmed
crossref
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 912
SubjectTerms 631/337/176/2016
631/337/2265
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Drug screening
Enhancers
Epigenesis, Genetic
Epigenetics
Fatty Acids
Ferroptosis
Ferroptosis - genetics
Immunology
Life Sciences
Lipid metabolism
Lipid Metabolism - genetics
Lipids
Metabolism
Mitochondria
Molecular modelling
Nuclear Proteins - metabolism
Oxidation
Polyunsaturated fatty acids
Transcription Factors - metabolism
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Title Bromodomain-containing protein 4 (BRD4) as an epigenetic regulator of fatty acid metabolism genes and ferroptosis
URI https://link.springer.com/article/10.1038/s41419-022-05344-0
https://www.ncbi.nlm.nih.gov/pubmed/36309482
https://www.proquest.com/docview/2729999926
https://www.proquest.com/docview/2730316764
https://pubmed.ncbi.nlm.nih.gov/PMC9617950
https://doaj.org/article/8c2a7e0671044bb19a7386fb02b67118
Volume 13
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