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Article ; Online: Metabolites and the tumour microenvironment: from cellular mechanisms to systemic metabolism.

Elia, Ilaria / Haigis, Marcia C

Nature metabolism

2021 Volume 3, Issue 1, Page(s) 21–32

Abstract: Metabolic transformation is a hallmark of cancer and a critical target for cancer therapy. Cancer metabolism and behaviour are regulated by cell-intrinsic factors as well as metabolite availability in the tumour microenvironment (TME). This metabolic ... ...

Abstract	Metabolic transformation is a hallmark of cancer and a critical target for cancer therapy. Cancer metabolism and behaviour are regulated by cell-intrinsic factors as well as metabolite availability in the tumour microenvironment (TME). This metabolic niche within the TME is shaped by four tiers of regulation: (1) intrinsic tumour cell metabolism, (2) interactions between cancer cells and non-cancerous cells, (3) tumour location and heterogeneity and (4) whole-body metabolic homeostasis. Here, we define these modes of metabolic regulation and review how distinct cell types contribute to the metabolite composition of the TME. Finally, we connect these insights to understand how each of these tiers offers unique therapeutic potential to modulate the metabolic profile and function of all cells inhabiting the TME.
MeSH term(s)	Gene Expression Regulation, Neoplastic/genetics ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Tumor Microenvironment/genetics
Language	English
Publishing date	2021-01-04
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-020-00317-z
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Article ; Online: Dangerous dynamic duo: Lactic acid and PD-1 blockade.

Johnson, Sheila / Haigis, Marcia C / Dougan, Stephanie K

Cancer cell

2022 Volume 40, Issue 2, Page(s) 127–130

Abstract: In this issue of Cancer Cell, Kumagai et al. reveal lactic acid as a mediator of checkpoint blockade resistance. Tumor-derived lactic acid promotes T regulatory cell (Treg) activity and impairs ... ...

Abstract	In this issue of Cancer Cell, Kumagai et al. reveal lactic acid as a mediator of checkpoint blockade resistance. Tumor-derived lactic acid promotes T regulatory cell (Treg) activity and impairs CD8
MeSH term(s)	CD8-Positive T-Lymphocytes/immunology ; Lactic Acid ; Programmed Cell Death 1 Receptor/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Programmed Cell Death 1 Receptor ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2022-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2022.01.008
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Zs.MG 104: Show issues

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Article ; Online: Nitrogen Metabolism in Cancer and Immunity.

Kurmi, Kiran / Haigis, Marcia C

Trends in cell biology

2020 Volume 30, Issue 5, Page(s) 408–424

Abstract: As one of the fundamental requirements for cell growth and proliferation, nitrogen acquisition and utilization must be tightly regulated. Nitrogen can be generated from amino acids (AAs) and utilized for biosynthetic processes through transamination and ... ...

Abstract	As one of the fundamental requirements for cell growth and proliferation, nitrogen acquisition and utilization must be tightly regulated. Nitrogen can be generated from amino acids (AAs) and utilized for biosynthetic processes through transamination and deamination reactions. Importantly, limitations of nitrogen availability in cells can disrupt the synthesis of proteins, nucleic acids, and other important nitrogen-containing compounds. Rewiring cellular metabolism to support anabolic processes is a feature common to both cancer and proliferating immune cells. In this review, we discuss how nitrogen is utilized in biosynthetic pathways and highlight different metabolic and oncogenic programs that alter the flow of nitrogen to sustain biomass production and growth, an important emerging feature of cancer and immune cell proliferation.
MeSH term(s)	Animals ; Humans ; Immunity ; Neoplasms/metabolism ; Nitrogen/metabolism ; Purines/metabolism ; Pyrimidines/metabolism ; Tumor Microenvironment
Chemical Substances	Purines ; Pyrimidines ; Nitrogen (N762921K75)
Language	English
Publishing date	2020-03-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2020.02.005
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Article ; Online: Regulatory T cells in dominant immunologic tolerance.

Georgiev, Peter / Benamar, Mehdi / Han, SeongJun / Haigis, Marcia C / Sharpe, Arlene H / Chatila, Talal A

The Journal of allergy and clinical immunology

2023 Volume 153, Issue 1, Page(s) 28–41

Abstract: Regulatory T cells expressing the transcription factor forkhead box protein 3 mediate peripheral immune tolerance both to self-antigens and to the commensal flora. Their defective function due to inborn errors of immunity or acquired insults is ... ...

Abstract	Regulatory T cells expressing the transcription factor forkhead box protein 3 mediate peripheral immune tolerance both to self-antigens and to the commensal flora. Their defective function due to inborn errors of immunity or acquired insults is associated with a broad range of autoimmune and immune dysregulatory diseases. Although their function in suppressing autoimmunity and enforcing commensalism is established, a broader role for regulatory T cells in tissue repair and metabolic regulation has emerged, enabled by unique programs of tissue adaptability and specialization. In this review, we focus on the myriad roles played by regulatory T cells in immunologic tolerance and host homeostasis and the potential to harness these cells in novel therapeutic approaches to human diseases.
MeSH term(s)	Humans ; T-Lymphocytes, Regulatory ; Immune Tolerance ; Immune System Diseases/metabolism ; Autoimmunity ; Forkhead Transcription Factors ; Autoimmune Diseases
Chemical Substances	Forkhead Transcription Factors
Language	English
Publishing date	2023-09-29
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2023.09.025
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Article ; Online: Sweet Temptation: From Sugar Metabolism to Gene Regulation.

Notarangelo, Giulia / Haigis, Marcia C

Immunity

2019 Volume 51, Issue 6, Page(s) 980–981

Abstract: In a recent issue of Nature, Zhang et al. (2019) describe an additional histone post-translational modification, named histone lactylation. Following increased lactate production as a consequence of M1 polarization, histone lactylation regulates the ... ...

Abstract	In a recent issue of Nature, Zhang et al. (2019) describe an additional histone post-translational modification, named histone lactylation. Following increased lactate production as a consequence of M1 polarization, histone lactylation regulates the induction of an M2-like phenotype in late stages of M1 macrophage activation to promote wound healing.
MeSH term(s)	Gene Expression Regulation ; Histones ; Macrophage Activation ; Macrophages ; Sugars
Chemical Substances	Histones ; Sugars
Language	English
Publishing date	2019-12-03
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2019.11.008
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 69: Show issues

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Article ; Online: SIRT4 loss reprograms intestinal nucleotide metabolism to support proliferation following perturbation of homeostasis.

Tucker, Sarah A / Hu, Song-Hua / Vyas, Sejal / Park, Albert / Joshi, Shakchhi / Inal, Aslihan / Lam, Tiffany / Tan, Emily / Haigis, Kevin M / Haigis, Marcia C

Cell reports

2024 Volume 43, Issue 4, Page(s) 113975

Abstract: The intestine is a highly metabolic tissue, but the metabolic programs that influence intestinal crypt proliferation, differentiation, and regeneration are still emerging. Here, we investigate how mitochondrial sirtuin 4 (SIRT4) affects intestinal ... ...

Abstract	The intestine is a highly metabolic tissue, but the metabolic programs that influence intestinal crypt proliferation, differentiation, and regeneration are still emerging. Here, we investigate how mitochondrial sirtuin 4 (SIRT4) affects intestinal homeostasis. Intestinal SIRT4 loss promotes cell proliferation in the intestine following ionizing radiation (IR). SIRT4 functions as a tumor suppressor in a mouse model of intestinal cancer, and SIRT4 loss drives dysregulated glutamine and nucleotide metabolism in intestinal adenomas. Intestinal organoids lacking SIRT4 display increased proliferation after IR stress, along with increased glutamine uptake and a shift toward de novo nucleotide biosynthesis over salvage pathways. Inhibition of de novo nucleotide biosynthesis diminishes the growth advantage of SIRT4-deficient organoids after IR stress. This work establishes SIRT4 as a modulator of intestinal metabolism and homeostasis in the setting of DNA-damaging stress.
MeSH term(s)	Animals ; Sirtuins/metabolism ; Homeostasis ; Cell Proliferation ; Mice ; Nucleotides/metabolism ; Intestines/pathology ; Organoids/metabolism ; Intestinal Mucosa/metabolism ; Glutamine/metabolism ; Humans ; Intestinal Neoplasms/metabolism ; Intestinal Neoplasms/pathology ; Intestinal Neoplasms/genetics ; Mice, Inbred C57BL ; Mitochondrial Proteins
Chemical Substances	Sirtuins (EC 3.5.1.-) ; Nucleotides ; SIRT4 protein, mouse (EC 3.5.1.-) ; Glutamine (0RH81L854J) ; Mitochondrial Proteins
Language	English
Publishing date	2024-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2024.113975
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Article ; Online: The multifaceted contributions of mitochondria to cellular metabolism.

Spinelli, Jessica B / Haigis, Marcia C

Nature cell biology

2018 Volume 20, Issue 7, Page(s) 745–754

Abstract: Although classically appreciated for their role as the powerhouse of the cell, the metabolic functions of mitochondria reach far beyond bioenergetics. In this Review, we discuss how mitochondria catabolize nutrients for energy, generate biosynthetic ... ...

Abstract	Although classically appreciated for their role as the powerhouse of the cell, the metabolic functions of mitochondria reach far beyond bioenergetics. In this Review, we discuss how mitochondria catabolize nutrients for energy, generate biosynthetic precursors for macromolecules, compartmentalize metabolites for the maintenance of redox homeostasis and function as hubs for metabolic waste management. We address the importance of these roles in both normal physiology and in disease.
MeSH term(s)	Animals ; Biological Transport ; Cell Survival ; Energy Metabolism ; Homeostasis ; Humans ; Mitochondria/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2018-06-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-018-0124-1
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Zs.MG 12: Show issues

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Article ; Online: The effects of age and systemic metabolism on anti-tumor T cell responses.

Drijvers, Jefte M / Sharpe, Arlene H / Haigis, Marcia C

eLife

2020 Volume 9

Abstract: Average age and obesity prevalence are increasing globally. Both aging and obesity are characterized by profound systemic metabolic and immunologic changes and are cancer risk factors. The mechanisms linking age and body weight to cancer are incompletely ...

Abstract	Average age and obesity prevalence are increasing globally. Both aging and obesity are characterized by profound systemic metabolic and immunologic changes and are cancer risk factors. The mechanisms linking age and body weight to cancer are incompletely understood, but recent studies have provided evidence that the anti-tumor immune response is reduced in both conditions, while responsiveness to immune checkpoint blockade, a form of cancer immunotherapy, is paradoxically intact. Dietary restriction, which promotes health and lifespan, may enhance cancer immunity. These findings illustrate that the systemic context can impact anti-tumor immunity and immunotherapy responsiveness. Here, we review the current knowledge of how age and systemic metabolic state affect the anti-tumor immune response, with an emphasis on CD8
MeSH term(s)	Age Factors ; Aging/immunology ; Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/physiology ; Humans ; Immunity/immunology ; Neoplasms/immunology ; Neoplasms/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/physiology
Keywords	covid19
Language	English
Publishing date	2020-11-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.62420
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Article ; Online: Lipid metabolism in sickness and in health: Emerging regulators of lipotoxicity.

Yoon, Haejin / Shaw, Jillian L / Haigis, Marcia C / Greka, Anna

Molecular cell

2021 Volume 81, Issue 18, Page(s) 3708–3730

Abstract: Lipids play crucial roles in signal transduction, contribute to the structural integrity of cellular membranes, and regulate energy metabolism. Questions remain as to which lipid species maintain metabolic homeostasis and which disrupt essential cellular ...

Abstract	Lipids play crucial roles in signal transduction, contribute to the structural integrity of cellular membranes, and regulate energy metabolism. Questions remain as to which lipid species maintain metabolic homeostasis and which disrupt essential cellular functions, leading to metabolic disorders. Here, we discuss recent advances in understanding lipid metabolism with a focus on catabolism, synthesis, and signaling. Technical advances, including functional genomics, metabolomics, lipidomics, lipid-protein interaction maps, and advances in mass spectrometry, have uncovered new ways to prioritize molecular mechanisms mediating lipid function. By reviewing what is known about the distinct effects of specific lipid species in physiological pathways, we provide a framework for understanding newly identified targets regulating lipid homeostasis with implications for ameliorating metabolic diseases.
MeSH term(s)	Animals ; Chromatin/metabolism ; Disease ; Energy Metabolism/physiology ; Health ; Homeostasis/physiology ; Humans ; Immunity/physiology ; Lipid Metabolism/physiology ; Lipidomics/methods ; Lipids/physiology ; Metabolic Diseases/metabolism ; Metabolic Diseases/physiopathology ; Metabolomics/methods ; Microbiota/physiology ; Signal Transduction/physiology
Chemical Substances	Chromatin ; Lipids
Language	English
Publishing date	2021-09-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.08.027
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Article ; Online: Age-associated remodeling of T cell immunity and metabolism.

Han, SeongJun / Georgiev, Peter / Ringel, Alison E / Sharpe, Arlene H / Haigis, Marcia C

Cell metabolism

2022 Volume 35, Issue 1, Page(s) 36–55

Abstract: Aging results in remodeling of T cell immunity and is associated with poor clinical outcomes in age-related diseases such as cancer. Among the hallmarks of aging, changes in host and cellular metabolism critically affect the development, maintenance, and ...

Abstract	Aging results in remodeling of T cell immunity and is associated with poor clinical outcomes in age-related diseases such as cancer. Among the hallmarks of aging, changes in host and cellular metabolism critically affect the development, maintenance, and function of T cells. Although metabolic perturbations impact anti-tumor T cell responses, the link between age-associated metabolic dysfunction and anti-tumor immunity remains unclear. In this review, we summarize recent advances in our understanding of aged T cell metabolism, with a focus on the bioenergetic and immunologic features of T cell subsets unique to the aging process. We also survey insights into mechanisms of metabolic T cell dysfunction in aging and discuss the impacts of aging on the efficacy of cancer immunotherapy. As the average life expectancy continues to increase, understanding the interplay between age-related metabolic reprogramming and maladaptive T cell immunity will be instrumental for the development of therapeutic strategies for older patients.
MeSH term(s)	Humans ; Aged ; T-Lymphocyte Subsets/metabolism ; Energy Metabolism ; Immunotherapy/methods ; Neoplasms/pathology ; Tumor Microenvironment
Language	English
Publishing date	2022-12-05
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2022.11.005
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