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      Role of p53 in the Regulation of Cellular Senescence

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          Abstract

          The p53 transcription factor plays a critical role in cellular responses to stress. Its activation in response to DNA damage leads to cell growth arrest, allowing for DNA repair, or directs cellular senescence or apoptosis, thereby maintaining genome integrity. Senescence is a permanent cell-cycle arrest that has a crucial role in aging, and it also represents a robust physiological antitumor response, which counteracts oncogenic insults. In addition, senescent cells can also negatively impact the surrounding tissue microenvironment and the neighboring cells by secreting pro-inflammatory cytokines, ultimately triggering tissue dysfunction and/or unfavorable outcomes. This review focuses on the characteristics of senescence and on the recent advances in the contribution of p53 to cellular senescence. Moreover, we also discuss the p53-mediated regulation of several pathophysiological microenvironments that could be associated with senescence and its development.

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          Cellular senescence in aging and age-related disease: from mechanisms to therapy.

          Bennett Childs, Matej Durik, Darren J. Baker … (2015)
          Cellular senescence, a process that imposes permanent proliferative arrest on cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related disease, and it is an attractive target for therapeutic exploitation. A wealth of information about senescence in cultured cells has been acquired over the past half century; however, senescence in living organisms is poorly understood, largely because of technical limitations relating to the identification and characterization of senescent cells in tissues and organs. Furthermore, newly recognized beneficial signaling functions of senescence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-aging therapy may have negative consequences. Here we discuss current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy.
          Article 0 comments Cited 842 times – based on 0 reviews     Review now
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            Forging a signature of in vivo senescence.

            Norman E. Sharpless, Charles J Sherr (2015)
            'Cellular senescence', a term originally defining the characteristics of cultured cells that exceed their replicative limit, has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. Proposed relationships between cellular senescence, tumour suppression, loss of tissue regenerative capacity and ageing suffer from lack of uniform definition and consistently applied criteria. Here, we highlight caveats in interpreting the importance of suboptimal senescence-associated biomarkers, expressed either alone or in combination. We advocate that more-specific descriptors be substituted for the now broadly applied umbrella term 'senescence' in defining the suite of diverse physiological responses to cellular stress.
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              Senescence in tumours: evidence from mice and humans.

              Manuel Collado, Manuel Serrano (2010)
              The importance of cellular senescence, which is a stress response that stably blocks proliferation, is increasingly being recognized. Senescence is prevalent in pre-malignant tumours, and progression to malignancy requires evading senescence. Malignant tumours, however, may still undergo senescence owing to interventions that restore tumour suppressor function or inactivate oncogenes. Senescent tumour cells can be cleared by immune cells, which may result in efficient tumour regression. Standard chemotherapy also has the potential to induce senescence, which may partly underlie its therapeutic activity. Although these concepts are well supported in mouse models, translating them to clinical oncology remains a challenge.
              Article 0 comments Cited 383 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomolecules
                Journal ID (iso-abbrev): Biomolecules
                Journal ID (publisher-id): biomolecules
                Title: Biomolecules
                Publisher: MDPI
                ISSN (Electronic): 2218-273X
                Publication date (Electronic): 08 March 2020
                Publication date Collection: March 2020
                Volume: 10
                Issue: 3
                Electronic Location Identifier: 420
                Affiliations
                [1 ]Sbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
                [2 ]Department of Medical Biotechnologies, University of Siena, 67100 Siena, Italy
                [3 ]Department of Life, Health and Environmental Sciences, University of L’Aquila, 53100 L’Aquila, Italy
                Author notes
                [* ]Correspondence: giordano@ 123456temple.edu
                Author information
                https://orcid.org/0000-0002-5959-016X
                Article
                Publisher ID: biomolecules-10-00420
                DOI: 10.3390/biom10030420
                PMC ID: 7175209
                PubMed ID: 32182711
                SO-VID: 9889ee7e-3877-4456-b1b7-30ddad682f8c
                Copyright © © 2020 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 : 31 January 2020
                Date accepted : 05 March 2020
                Categories
                Subject: Review

                Keywords: p53,senescence,cell cycle arrest,microenvironment,dna damage
                Data availability:
                Keywords: p53, senescence, cell cycle arrest, microenvironment, dna damage

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