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  1. Article ; Online: Fatty acids prime the lung as a site for tumour spread.

    Pinheiro, Laura V / Wellen, Kathryn E

    Nature

    2023  Volume 615, Issue 7951, Page(s) 224–225

    MeSH term(s) Humans ; Fatty Acids ; Neoplasms ; Lung
    Chemical Substances Fatty Acids
    Language English
    Publishing date 2023-03-15
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-023-00538-8
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  2. Article ; Online: Acetyl-CoA metabolism in cancer.

    Guertin, David A / Wellen, Kathryn E

    Nature reviews. Cancer

    2023  Volume 23, Issue 3, Page(s) 156–172

    Abstract: Few metabolites can claim a more central and versatile role in cell metabolism than acetyl coenzyme A (acetyl-CoA). Acetyl-CoA is produced during nutrient catabolism to fuel the tricarboxylic acid cycle and is the essential building block for fatty acid ... ...

    Abstract Few metabolites can claim a more central and versatile role in cell metabolism than acetyl coenzyme A (acetyl-CoA). Acetyl-CoA is produced during nutrient catabolism to fuel the tricarboxylic acid cycle and is the essential building block for fatty acid and isoprenoid biosynthesis. It also functions as a signalling metabolite as the substrate for lysine acetylation reactions, enabling the modulation of protein functions in response to acetyl-CoA availability. Recent years have seen exciting advances in our understanding of acetyl-CoA metabolism in normal physiology and in cancer, buoyed by new mouse models, in vivo stable-isotope tracing approaches and improved methods for measuring acetyl-CoA, including in specific subcellular compartments. Efforts to target acetyl-CoA metabolic enzymes are also advancing, with one therapeutic agent targeting acetyl-CoA synthesis receiving approval from the US Food and Drug Administration. In this Review, we give an overview of the regulation and cancer relevance of major metabolic pathways in which acetyl-CoA participates. We further discuss recent advances in understanding acetyl-CoA metabolism in normal tissues and tumours and the potential for targeting these pathways therapeutically. We conclude with a commentary on emerging nodes of acetyl-CoA metabolism that may impact cancer biology.
    MeSH term(s) Animals ; Humans ; Mice ; Acetyl Coenzyme A/metabolism ; Metabolic Networks and Pathways ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Disease Models, Animal
    Chemical Substances Acetyl Coenzyme A (72-89-9)
    Language English
    Publishing date 2023-01-19
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/s41568-022-00543-5
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  3. Article ; Online: Advances into understanding metabolites as signaling molecules in cancer progression.

    Liu, Joyce Y / Wellen, Kathryn E

    Current opinion in cell biology

    2020  Volume 63, Page(s) 144–153

    Abstract: Recent years have seen a great expansion in our knowledge of the roles that metabolites play in cellular signaling. Structural data have provided crucial insights into mechanisms through which amino acids are sensed. New nutrient-coupled protein and RNA ... ...

    Abstract Recent years have seen a great expansion in our knowledge of the roles that metabolites play in cellular signaling. Structural data have provided crucial insights into mechanisms through which amino acids are sensed. New nutrient-coupled protein and RNA modifications have been identified and characterized. A growing list of functions has been ascribed to metabolic regulation of modifications such as acetylation, methylation, and glycosylation. A current challenge lies in developing an integrated understanding of the roles that metabolic signaling mechanisms play in physiology and disease, which will inform the design of strategies to target such mechanisms. In this brief article, we review recent advances in metabolic signaling through post-translational modification during cancer progression, to provide a framework for understanding signaling roles of metabolites in the context of cancer biology and illuminate areas for future investigation.
    MeSH term(s) Acetylation ; Animals ; Disease Progression ; Glycosylation ; Humans ; Metabolome/physiology ; Methylation ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Protein Processing, Post-Translational/physiology ; Signal Transduction/genetics
    Chemical Substances Neoplasm Proteins
    Language English
    Publishing date 2020-02-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1026381-0
    ISSN 1879-0410 ; 0955-0674
    ISSN (online) 1879-0410
    ISSN 0955-0674
    DOI 10.1016/j.ceb.2020.01.013
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  4. Article ; Online: Histone lactylation links metabolism and gene regulation.

    Izzo, Luke T / Wellen, Kathryn E

    Nature

    2019  Volume 574, Issue 7779, Page(s) 492–493

    MeSH term(s) Chromatin ; Gene Expression Regulation ; Histones
    Chemical Substances Chromatin ; Histones
    Language English
    Publishing date 2019-10-23
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-019-03122-1
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  5. Article ; Online: Epigenetic Control of Fatty-Acid Metabolism Sustains Glioma Stem Cells.

    Affronti, Hayley C / Wellen, Kathryn E

    Cancer discovery

    2019  Volume 9, Issue 9, Page(s) 1161–1163

    Abstract: In this issue ... ...

    Abstract In this issue of
    MeSH term(s) Epigenesis, Genetic ; ErbB Receptors ; Glioblastoma/genetics ; Glioma ; Humans ; Neoplastic Stem Cells
    Chemical Substances EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2019-09-02
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-19-0733
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  6. Article ; Online: Metabolite regulates differentiation.

    Trefely, Sophie / Wellen, Kathryn E

    Science (New York, N.Y.)

    2018  Volume 360, Issue 6389, Page(s) 603–604

    MeSH term(s) Cell Differentiation
    Language English
    Publishing date 2018--11
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aat6663
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  7. Article ; Online: Should we consider subcellular compartmentalization of metabolites, and if so, how do we measure them?

    Wellen, Kathryn E / Snyder, Nathaniel W

    Current opinion in clinical nutrition and metabolic care

    2019  Volume 22, Issue 5, Page(s) 347–354

    Abstract: Purpose of review: To examine the consequences of metabolism compartmentalized at the subcellular level, provide prototypical examples of compartmentalized metabolism, and describe methods to examine compartmentalized metabolism.: Recent findings: ... ...

    Abstract Purpose of review: To examine the consequences of metabolism compartmentalized at the subcellular level, provide prototypical examples of compartmentalized metabolism, and describe methods to examine compartmentalized metabolism.
    Recent findings: Progress in metabolomics and isotope tracing has underscored the importance of subcellular compartments of metabolism. The discovery of biological effects of metabolites as bioenergetic intermediates, anabolic building blocks, signaling mediators, and effectors in posttranslation modifications of proteins and nucleic acids have highlighted the role of compartmentalization in determining metabolic fate. Recent advances in both direct and indirect methods to quantify compartmentalized metabolism have improved upon historical approaches. Genetically encoded metabolite sensors, chemical probes, immunoaffinity purification, and compartment-resolved metabolic modeling have all been recently applied to study compartmentalization.
    Summary: Accurate measurement of metabolites in distinct subcellular compartments is important for understanding and pharmacologically targeting metabolic pathways in diverse disease contexts, including cancer, diabetes, heart failure, obesity, and regulation of the immune system. Direct and indirect approaches to quantify compartmentalized metabolism are advancing rapidly. Yet, major challenges remain in the generalizability, rigor, and interpretation of data from the available methods to quantify compartmentalized metabolism.
    MeSH term(s) Animals ; Cell Compartmentation/physiology ; Intracellular Space/chemistry ; Intracellular Space/metabolism ; Isotope Labeling ; Metabolic Networks and Pathways/physiology ; Metabolomics/methods ; Mice ; Mitochondria/chemistry ; Mitochondria/metabolism
    Language English
    Publishing date 2019-07-31
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1460178-3
    ISSN 1473-6519 ; 1363-1950
    ISSN (online) 1473-6519
    ISSN 1363-1950
    DOI 10.1097/MCO.0000000000000580
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  8. Article ; Online: The interaction between the gut microbiota and dietary carbohydrates in nonalcoholic fatty liver disease.

    Park, Grace / Jung, Sunhee / Wellen, Kathryn E / Jang, Cholsoon

    Experimental & molecular medicine

    2021  Volume 53, Issue 5, Page(s) 809–822

    Abstract: Imbalance between fat production and consumption causes various metabolic disorders. Nonalcoholic fatty liver disease (NAFLD), one such pathology, is characterized by abnormally increased fat synthesis and subsequent fat accumulation in ... ...

    Abstract Imbalance between fat production and consumption causes various metabolic disorders. Nonalcoholic fatty liver disease (NAFLD), one such pathology, is characterized by abnormally increased fat synthesis and subsequent fat accumulation in hepatocytes
    MeSH term(s) Animals ; Biomarkers ; Carbohydrate Metabolism ; Comorbidity ; Dietary Carbohydrates/metabolism ; Disease Susceptibility ; Fructose/metabolism ; Gastrointestinal Microbiome ; Gene Expression Regulation, Enzymologic ; Host Microbial Interactions ; Humans ; Insulin Resistance ; Lipid Metabolism ; Liver/metabolism ; Liver/pathology ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology
    Chemical Substances Biomarkers ; Dietary Carbohydrates ; Fructose (30237-26-4)
    Language English
    Publishing date 2021-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-021-00614-x
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  9. Article: The Bidirectional Relationship Between Cancer Epigenetics and Metabolism.

    Izzo, Luke T / Affronti, Hayley C / Wellen, Kathryn E

    Annual review of cancer biology

    2020  Volume 5, Issue 1, Page(s) 235–257

    Abstract: Metabolic and epigenetic reprogramming are characteristics of cancer cells that, in many cases, are linked. Oncogenic signaling, diet, and tumor microenvironment each influence the availability of metabolites that are substrates or inhibitors of ... ...

    Abstract Metabolic and epigenetic reprogramming are characteristics of cancer cells that, in many cases, are linked. Oncogenic signaling, diet, and tumor microenvironment each influence the availability of metabolites that are substrates or inhibitors of epigenetic enzymes. Reciprocally, altered expression or activity of chromatin-modifying enzymes can exert direct and indirect effects on cellular metabolism. In this article, we discuss the bidirectional relationship between epigenetics and metabolism in cancer. First, we focus on epigenetic control of metabolism, highlighting evidence that alterations in histone modifications, chromatin remodeling, or the enhancer landscape can drive metabolic features that support growth and proliferation. We then discuss metabolic regulation of chromatin-modifying enzymes and roles in tumor growth and progression. Throughout, we highlight proposed therapeutic and dietary interventions that leverage metabolic-epigenetic cross talk and have the potential to improve cancer therapy.
    Language English
    Publishing date 2020-11-30
    Publishing country United States
    Document type Journal Article
    ISSN 2472-3428
    ISSN 2472-3428
    DOI 10.1146/annurev-cancerbio-070820-035832
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  10. Article ; Online: Metabolic Signaling to the Nucleus in Cancer.

    Campbell, Sydney L / Wellen, Kathryn E

    Molecular cell

    2018  Volume 71, Issue 3, Page(s) 398–408

    Abstract: Nutrient-sensing mechanisms ensure that cellular activities are coordinated with nutrient availability. Recent work has established links between metabolite pools and protein post-translational modifications, as metabolites are substrates of enzymes that ...

    Abstract Nutrient-sensing mechanisms ensure that cellular activities are coordinated with nutrient availability. Recent work has established links between metabolite pools and protein post-translational modifications, as metabolites are substrates of enzymes that add or remove modifications such as acetylation, methylation, and glycosylation. Cancer cells undergo metabolic reprogramming and exhibit metabolic plasticity that allows them to survive and proliferate within the tumor microenvironment. In this article we review the evidence that, in cancer cells, nutrient availability and oncogenic metabolic reprogramming impact the abundance of key metabolites that regulate signaling and epigenetics. We propose models to explain how these metabolites may control locus-specific chromatin modification and gene expression. Finally, we discuss emerging roles of metabolites in regulating malignant phenotypes and tumorigenesis via transcriptional control. An improved understanding of how metabolic alterations in cancer affect nuclear gene regulation could uncover new vulnerabilities to target therapeutically.
    MeSH term(s) Acetylation ; Animals ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Cell Nucleus/metabolism ; Epigenesis, Genetic/genetics ; Epigenomics ; Gene Expression Regulation, Neoplastic/genetics ; Histones/metabolism ; Humans ; Metabolic Networks and Pathways/physiology ; Methylation ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Nutrients/metabolism ; Nutrigenomics ; Protein Processing, Post-Translational ; Signal Transduction
    Chemical Substances Histones ; Nutrients
    Language English
    Publishing date 2018-08-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2018.07.015
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