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      Multifaceted Role of PARP-1 in DNA Repair and Inflammation: Pathological and Therapeutic Implications in Cancer and Non-Cancer Diseases

      review-article
      Author(s): * , *
      Publication date (Electronic):
      Journal: Cells
      Publisher: MDPI
      Keywords: PARP, inflammation, tumor, DNA repair, PARP inhibitors

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          Abstract

          PARP-1 (poly(ADP-ribose)-polymerase 1), mainly known for its protective role in DNA repair, also regulates inflammatory processes. Notably, defects in DNA repair and chronic inflammation may both predispose to cancer development. On the other hand, inhibition of DNA repair and inflammatory responses can be beneficial in cancer therapy and PARP inhibitors are currently used for their lethal effects on tumor cells. Furthermore, excess of PARP-1 activity has been associated with many tumors and inflammation-related clinical conditions, including asthma, sepsis, arthritis, atherosclerosis, and neurodegenerative diseases, to name a few. Activation and inhibition of PARP represent, therefore, a double-edged sword that can be exploited for therapeutic purposes. In our review, we will discuss recent findings highlighting the composite multifaceted role of PARP-1 in cancer and inflammation-related diseases.

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          DAMP-sensing receptors in sterile inflammation and inflammatory diseases

          Tao Gong, Lei Liu, Wei Jiang … (2019)
          The innate immune system has the capacity to detect 'non-self' molecules derived from pathogens, known as pathogen-associated molecular patterns, via pattern recognition receptors. In addition, an increasing number of endogenous host-derived molecules, termed damage-associated molecular patterns (DAMPs), have been found to be sensed by various innate immune receptors. The recognition of DAMPs, which are produced or released by damaged and dying cells, promotes sterile inflammation, which is important for tissue repair and regeneration, but can also lead to the development of numerous inflammatory diseases, such as metabolic disorders, neurodegenerative diseases, autoimmune diseases and cancer. Here we examine recent discoveries concerning the roles of DAMP-sensing receptors in sterile inflammation and in diseases resulting from dysregulated sterile inflammation, and then discuss insights into the cross-regulation of these receptors and their ligands.
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            Mediation of poly(ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor.

            Seong-Woon Yu, Hongmin Wang, Marc F Poitras … (2002)
            Poly(ADP-ribose) polymerase-1 (PARP-1) protects the genome by functioning in the DNA damage surveillance network. PARP-1 is also a mediator of cell death after ischemia-reperfusion injury, glutamate excitotoxicity, and various inflammatory processes. We show that PARP-1 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and that AIF is necessary for PARP-1-dependent cell death. N-methyl-N'-nitro-N-nitrosoguanidine, H2O2, and N-methyl-d-aspartate induce AIF translocation and cell death, which is prevented by PARP inhibitors or genetic knockout of PARP-1, but is caspase independent. Microinjection of an antibody to AIF protects against PARP-1-dependent cytotoxicity. These data support a model in which PARP-1 activation signals AIF release from mitochondria, resulting in a caspase-independent pathway of programmed cell death.
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              The PARP side of the nucleus: molecular actions, physiological outcomes, and clinical targets.

              Raga Krishnakumar, W. Kraus (2010)
              The abundant nuclear enzyme PARP-1, a multifunctional regulator of chromatin structure, transcription, and genomic integrity, plays key roles in a wide variety of processes in the nucleus. Recent studies have begun to connect the molecular functions of PARP-1 to specific physiological and pathological outcomes, many of which can be altered by an expanding array of chemical inhibitors of PARP enzymatic activity. 2010 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 266 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 22 December 2019
                Publication date Collection: January 2020
                Volume: 9
                Issue: 1
                Electronic Location Identifier: 41
                Affiliations
                ENEA, Laboratory of Biomedical Technologies, 00123 Rome, Italy
                Author notes
                [* ]Correspondence: simonetta.pazzaglia@ 123456enea.it (S.P.); claudio.pioli@ 123456enea.it (C.P.); Tel.: +39-06-3048-6535 (S.P.); +39-06-3048-3398 (C.P.)
                Author information
                https://orcid.org/0000-0002-1360-2727
                Article
                Publisher ID: cells-09-00041
                DOI: 10.3390/cells9010041
                PMC ID: 7017201
                PubMed ID: 31877876
                SO-VID: dd9edd0a-bb37-4a4b-ba15-475848b15293
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 November 2019
                Date accepted : 20 December 2019
                Categories
                Subject: Review

                Keywords: parp,inflammation,tumor,dna repair,parp inhibitors
                Data availability:
                Keywords: parp, inflammation, tumor, dna repair, parp inhibitors

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