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      Histone lactylation bridges metabolic reprogramming and epigenetic rewiring in driving carcinogenesis: Oncometabolite fuels oncogenic transcription

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          Abstract

          Heightened lactate production in cancer cells has been linked to various cellular mechanisms such as angiogenesis, hypoxia, macrophage polarisation and T‐cell dysfunction. The lactate‐induced lactylation of histone lysine residues is noteworthy, as it functions as an epigenetic modification that directly augments gene transcription from chromatin. This epigenetic modification originating from lactate effectively fosters a reliance on transcription, thereby expediting tumour progression and development. Herein, this review explores the correlation between histone lactylation and cancer characteristics, revealing histone lactylation as an innovative epigenetic process that enhances the vulnerability of cells to malignancy. Moreover, it is imperative to acknowledge the paramount importance of acknowledging innovative therapeutic methodologies for proficiently managing cancer by precisely targeting lactate signalling. This comprehensive review illuminates a crucial yet inadequately investigated aspect of histone lactylation, providing valuable insights into its clinical ramifications and prospective therapeutic interventions centred on lactylation.

          Abstract

          1. The lactate‐induced lactylation of histone lysine residues bridges the metabolic reprogramming and epigenetic rewiring.

          2. Histone lactylation fuels oncogene overexpression, expediting tumour progression and development.

          3. Targeting lactate signalling exhibits with therapeutic efficacy in diversified cancers.

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          Most cited references148

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          Understanding the Warburg effect: the metabolic requirements of cell proliferation.

          Craig B Thompson, Matthew Vander Heiden, Lewis Cantley (2009)
          In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5'-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer.
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            Metabolic regulation of gene expression by histone lactylation

            Di Zhang, Zhanyun Tang, He Huang … (2019)
            The Warburg effect, originally describing augmented lactogenesis in cancer, is associated with diverse cellular processes such as angiogenesis, hypoxia, macrophage polarization, and T-cell activation. This phenomenon is intimately linked with multiple diseases including neoplasia, sepsis, and autoimmune diseases 1,2 . Lactate, a compound generated during Warburg effect, is widely known as an energy source and metabolic byproduct. However, its non-metabolic functions in physiology and disease remain unknown. Here we report lactate-derived histone lysine lactylation as a new epigenetic modification and demonstrate that histone lactylation directly stimulates gene transcription from chromatin. In total, we identify 28 lactylation sites on core histones in human and mouse cells. Hypoxia and bacterial challenges induce production of lactate through glycolysis that in turn serves as precursor for stimulating histone lactylation. Using bacterially exposed M1 macrophages as a model system, we demonstrate that histone lactylation has different temporal dynamics from acetylation. In the late phase of M1 macrophage polarization, elevated histone lactylation induces homeostatic genes involved in wound healing including arginase 1. Collectively, our results suggest the presence of an endogenous “lactate clock” in bacterially challenged M1 macrophages that turns on gene expression to promote homeostasis. Histone lactylation thus represents a new avenue for understanding the functions of lactate and its role in diverse pathophysiological conditions, including infection and cancer.
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              Metabolic reprogramming: a cancer hallmark even warburg did not anticipate.

              Patrick Ward, Craig B Thompson (2012)
              Cancer metabolism has long been equated with aerobic glycolysis, seen by early biochemists as primitive and inefficient. Despite these early beliefs, the metabolic signatures of cancer cells are not passive responses to damaged mitochondria but result from oncogene-directed metabolic reprogramming required to support anabolic growth. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular differentiation. No longer can cancer-associated alterations in metabolism be viewed as an indirect response to cell proliferation and survival signals. We contend that altered metabolism has attained the status of a core hallmark of cancer. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Meili Li: limeili0319@163.com
                Peirong Lu:
                ORCID: https://orcid.org/0000-0002-1423-1737
                lupeirong@suda.edu.cn
                Journal
                Journal ID (nlm-ta): Clin Transl Med
                Journal ID (iso-abbrev): Clin Transl Med
                Journal ID (doi): 10.1002/(ISSN)2001-1326
                Journal ID (publisher-id): CTM2
                Title: Clinical and Translational Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2001-1326
                Publication date (Electronic): 08 March 2024
                Publication date Collection: March 2024
                Volume: 14
                Issue: 3 ( doiID: 10.1002/ctm2.v14.3 )
                Electronic Location Identifier: e1614
                Affiliations
                [ 1 ] Department of Clinical Medicine Xuzhou Medical University Xuzhou Jiangsu China
                [ 2 ] Department of Ophthalmology Peking Union Medical College Hospital Beijing China
                [ 3 ] Department of Ophthalmology Eye Disease Prevention and Treatment Institute of Xuzhou, The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University Xuzhou First People's Hospital Xuzhou Jiangsu China
                [ 4 ] Department of Ophthalmology The First Affiliated Hospital of Soochow University Suzhou China
                Author notes
                [*] [* ] Correspondence

                Meili Li, Department of Ophthalmology, Eye Disease Prevention and Treatment Institute of Xuzhou, The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, Xuzhou First People's Hospital, No. 269 Daxue Road, Xuzhou, Jiangsu, China.

                Email: limeili0319@ 123456163.com

                Peirong Lu, Department of Ophthalmology, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, China.

                Email: lupeirong@ 123456suda.edu.cn

                Author information
                https://orcid.org/0000-0002-1423-1737
                Article
                Publisher ID: CTM21614
                DOI: 10.1002/ctm2.1614
                PMC ID: 10921234
                PubMed ID: 38456209
                SO-VID: a1388272-4079-4085-9fc9-57807e2c809a
                Copyright © © 2024 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date revision received : 13 February 2024
                Date received : 05 December 2023
                Date accepted : 18 February 2024
                Page count
                Figures: 5, Tables: 2, Pages: 15, Words: 9263
                Funding
                Funded by: Suzhou Municipal Health Commission , doi 10.13039/100018916;
                Award ID: KJXW2020077
                Funded by: Science and Technology Program of Suzhou , doi 10.13039/501100018556;
                Award ID: SKJY2021015
                Award ID: SYSD2020048
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                cover-date March 2024
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.9 mode:remove_FC converted:08.03.2024

                ScienceOpen disciplines: Medicine
                Keywords: cancer,histone lactylation,metabolic reprogramming
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: cancer, histone lactylation, metabolic reprogramming

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