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      The role of UV-DDB in processing 8-oxoguanine during base excision repair

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          Abstract

          Recent data from our laboratory has shown that the nucleotide excision repair (NER) proteins UV-damaged DNA-binding protein (UV-DDB), xeroderma pigmentosum group C (XPC), and xeroderma pigmentosum group A (XPA) play important roles in the processing of 8-oxoG. This review first discusses biochemical studies demonstrating how UV-DDB stimulates human 8-oxoG glycosylase (OGG1), MUTYH, and apurinic/apyrimidinic (AP) endonuclease (APE1) to increase their turnover at damage sites. We further discuss our single-molecule studies showing that UV-DDB associates with these proteins at abasic moieties on DNA damage arrays. Data from cell experiments are then described showing that UV-DDB interacts with OGG1 at sites of 8-oxoG. Finally, since many glycosylases are inhibited from working on damage in the context of chromatin, we present a working model of how UV-DDB may be the first responder to alter the structure of damage containing-nucleosomes to allow access by base excision repair (BER) enzymes.

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          Oxidative stress, inflammation, and cancer: how are they linked?

          Simone Reuter, Subash C Gupta, Madan Chaturvedi … (2010)
          Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer, diabetes, and cardiovascular, neurological, and pulmonary diseases. Oxidative stress can activate a variety of transcription factors including NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. Activation of these transcription factors can lead to the expression of over 500 different genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. How oxidative stress activates inflammatory pathways leading to transformation of a normal cell to tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival is the focus of this review. Overall, observations to date suggest that oxidative stress, chronic inflammation, and cancer are closely linked. Copyright © 2010 Elsevier Inc. All rights reserved.
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            Endogenous DNA Damage as a Source of Genomic Instability in Cancer

            Anthony T. Tubbs, André Nussenzweig (2017)
            Genome instability, defined as higher than normal rates of mutation, is a double-edged sword. As a source of genetic diversity and natural selection, mutations are beneficial for evolution. On the other hand, genomic instability can have catastrophic consequences for age-related diseases such as cancer. Mutations arise either from inactivation of DNA repair pathways or in a repair-competent background due to genotoxic stress from celluar processes such as transcription and replication that overwhelm high-fidelity DNA repair. Here, we review recent studies that shed light on endogenous sources of mutation and epigenomic features that promote genomic instability during cancer evolution.
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              Understanding nucleotide excision repair and its roles in cancer and ageing.

              Jan H. J. Hoeijmakers, Hannes Lans, Wim Vermeulen … (2014)
              Nucleotide excision repair (NER) eliminates various structurally unrelated DNA lesions by a multiwise 'cut and patch'-type reaction. The global genome NER (GG-NER) subpathway prevents mutagenesis by probing the genome for helix-distorting lesions, whereas transcription-coupled NER (TC-NER) removes transcription-blocking lesions to permit unperturbed gene expression, thereby preventing cell death. Consequently, defects in GG-NER result in cancer predisposition, whereas defects in TC-NER cause a variety of diseases ranging from ultraviolet radiation-sensitive syndrome to severe premature ageing conditions such as Cockayne syndrome. Recent studies have uncovered new aspects of DNA-damage detection by NER, how NER is regulated by extensive post-translational modifications, and the dynamic chromatin interactions that control its efficiency. Based on these findings, a mechanistic model is proposed that explains the complex genotype-phenotype correlations of transcription-coupled repair disorders.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biochem Soc Trans
                Journal ID (iso-abbrev): Biochem Soc Trans
                Journal ID (publisher-id): BST
                Title: Biochemical Society Transactions
                Publisher: Portland Press Ltd.
                ISSN (Print): 0300-5127
                ISSN (Electronic): 1470-8752
                Publication date (Print): 31 October 2022
                Publication date (Electronic): 28 October 2022
                Volume: 50
                Issue: 5
                Pages: 1481-1488
                Affiliations
                [1 ]UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213, U.S.A.
                [2 ]Department of Pharmacology and Chemical Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, U.S.A.
                Author notes
                Correspondence: Bennett Van Houten ( vanhoutenb@ 123456upmc.edu )
                Author information
                http://orcid.org/0000-0002-4009-2478
                Article
                Publisher ID: BST-50-1481
                DOI: 10.1042/BST20220748
                PMC ID: 9704513
                PubMed ID: 36305644
                SO-VID: 4850988e-cb7b-400d-83ae-8d27e7e03068
                Copyright © © 2022 The Author(s)
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND).

                History
                Date received : 8 August 2022
                Date revision received : 4 October 2022
                Date accepted : 10 October 2022
                Categories
                Subject: Cancer
                Subject: Biophysics
                Subject: Aging
                Subject: Molecular Interactions
                Subject: Mutation
                Subject: Review Articles

                ScienceOpen disciplines: Biochemistry
                Keywords: 8-oxoguanine,base excision repair,nucleotide excision repair,ogg1,uv-ddb
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: 8-oxoguanine, base excision repair, nucleotide excision repair, ogg1, uv-ddb

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