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      The interconnected roles of TRIM21/Ro52 in systemic lupus erythematosus, primary Sjögren’s syndrome, cancers, and cancer metabolism

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          Abstract

          Protein tripartite motif-containing 21 (TRIM21/Ro52), an E3 ubiquitin ligase, is an essential regulator of innate immunity, and its dysregulation is closely associated with the development of autoimmune diseases, predominantly systemic lupus erythematosus (SLE) and primary Sjögren’s syndrome (pSS). TRIM21 /Ro52 also features anti-cancer and carcinogenic functions according to different malignancies. The interconnected role of TRIM21/Ro52 in regulating autoimmunity and cell metabolism in autoimmune diseases and malignancies is implicated. In this review, we summarize current findings on how TRIM21/Ro52 affects inflammation and tumorigenesis, and investigate the relationship between TRIM21/Ro52 expression and the formation of lymphoma and breast cancer in SLE and pSS populations.

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          Hallmarks of Cancer: The Next Generation

          Douglas Hanahan, Robert A. Weinberg (2011)
          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Understanding the Warburg effect: the metabolic requirements of cell proliferation.

            Matthew G Vander Heiden, Lewis C Cantley, Craig B Thompson (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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              Oxidative Stress in Cancer

              John Hayes, Albena T. Dinkova-Kostova, Kenneth D. Tew (2020)
              Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation, and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.
              Article 0 comments Cited 702 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yung-Luen Yu: ylyu@mail.cmu.edu.tw
                Journal
                Journal ID (nlm-ta): Cancer Cell Int
                Journal ID (iso-abbrev): Cancer Cell Int
                Title: Cancer Cell International
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1475-2867
                Publication date (Electronic): 22 November 2023
                Publication date PMC-release: 22 November 2023
                Publication date Collection: 2023
                Volume: 23
                Electronic Location Identifier: 289
                Affiliations
                [1 ]Graduate Institute of Biomedical Sciences, College of Medicine, China Medical University, ( https://ror.org/00v408z34) Taichung, 40402 Taiwan
                [2 ]Institute of Translational Medicine and New Drug Development, Taichung, 40402 Taiwan
                [3 ]Center for Molecular Medicine, China Medical University Hospital, ( https://ror.org/0368s4g32) Taichung, 40402 Taiwan
                [4 ]Department of Medical Laboratory Science and Biotechnology, Asia University, ( https://ror.org/03z7kp760) Taichung, 41354 Taiwan
                Article
                Publisher ID: 3143
                DOI: 10.1186/s12935-023-03143-x
                PMC ID: 10664372
                SO-VID: dc04e4cd-7e19-42ce-ba19-891a71524fde
                Copyright © © The Author(s) 2023
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 30 July 2023
                Date accepted : 13 November 2023
                Funding
                Funded by: National Science and Technology Council, Taiwan
                Award ID: NSTC 110-2314-B-039-034-MY3
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © BioMed Central Ltd., part of Springer Nature 2023

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: trim21/ro52,anti-ro52 antibody,systemic lupus erythematosus,primary sjögren’s syndrome,cancer immunology,cancer metabolism
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: trim21/ro52, anti-ro52 antibody, systemic lupus erythematosus, primary sjögren’s syndrome, cancer immunology, cancer metabolism

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