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      Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging

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      Publication date (Electronic):
      Journal: Aging (Albany NY)
      Publisher: Impact Journals LLC
      Keywords: senescence, geroconversion, gerosuppressants, rapamycin, mTOR

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          Abstract

          Cell cycle arrest is not yet senescence. When the cell cycle is arrested, an inappropriate growth-promotion converts an arrest into senescence (geroconversion). By inhibiting the growth-promoting mTOR pathway, rapamycin decelerates geroconversion of the arrested cells. And as a striking example, while causing arrest, p53 may decelerate or suppress geroconversion (in some conditions). Here I discuss the meaning of geroconversion and also the terms gerogenes, gerossuppressors, gerosuppressants, gerogenic pathways, gero-promoters, hyperfunction and feedback resistance, regenerative potential, hypertrophy and secondary atrophy, pro-gerogenic and gerogenic cells.

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          Cancer genes and the pathways they control.

          Bert Vogelstein, Kenneth W. Kinzler (2004)
          The revolution in cancer research can be summed up in a single sentence: cancer is, in essence, a genetic disease. In the last decade, many important genes responsible for the genesis of various cancers have been discovered, their mutations precisely identified, and the pathways through which they act characterized. The purposes of this review are to highlight examples of progress in these areas, indicate where knowledge is scarce and point out fertile grounds for future investigation.
          Article 0 comments Cited 950 times – based on 0 reviews     Review now
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            Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion

            Francis Rodier, Jean-Philippe Coppe, Christopher K Patil … (2009)
            Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells1. Paradoxically, senescent cells also secrete factors that alter tissue microenvironments2. The pathways regulating this secretion are unknown. We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks (DSBs), which initiate increased secretion of inflammatory cytokines such as interleukin-6 (IL-6). Cytokine secretion occurred only after establishment of persistent DNA damage signaling, usually associated with senescence, not after transient DNA damage responses (DDR). Initiation and maintenance of this cytokine response required the DDR proteins ATM, NBS1 and CHK2, but not the cell cycle arrest enforcers p53 and pRb. ATM was also essential for IL-6 secretion during oncogene-induced senescence and by damaged cells that bypass senescence. Further, DDR activity and IL-6 were elevated in human cancers, and ATM-depletion suppressed the ability of senescent cells to stimulate IL-6-dependent cancer cell invasiveness. Thus, in addition to orchestrating cell cycle checkpoints and DNA repair, a novel and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue.
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              Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.

              M. Serrano, A. Lin, M. McCurrach … (1997)
              Oncogenic ras can transform most immortal rodent cells to a tumorigenic state. However, transformation of primary cells by ras requires either a cooperating oncogene or the inactivation of tumor suppressors such as p53 or p16. Here we show that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest. The arrest induced by ras is accompanied by accumulation of p53 and p16, and is phenotypically indistinguishable from cellular senescence. Inactivation of either p53 or p16 prevents ras-induced arrest in rodent cells, and E1A achieves a similar effect in human cells. These observations suggest that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an oncogenic stimulus. Negation of ras-induced senescence may be relevant during multistep tumorigenesis.
              Article 0 comments Cited 632 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Aging (Albany NY)
                Journal ID (iso-abbrev): Aging (Albany NY)
                Journal ID (publisher-id): ImpactJ
                Title: Aging (Albany NY)
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1945-4589
                Publication date Collection: March 2012
                Publication date (Electronic): 5 March 2012
                Volume: 4
                Issue: 3
                Pages: 159-165
                Affiliations
                Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3-312, Buffalo, NY, 14263, USA
                Author notes
                Correspondence to: Mikhail V. Blagosklonny, MD/PhD ; blagosklonny@ 123456oncotarget.com
                Article
                DOI: 10.18632/aging.100443
                PMC ID: 3348476
                PubMed ID: 22394614
                SO-VID: 7e92b9af-6a9e-4d6c-8d44-1a71a825544c
                Copyright © Copyright: © 2012 Blagosklonny
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                Date received : 17 February 2012
                Date accepted : 5 March 2012
                Categories
                Subject: Research Perspective

                ScienceOpen disciplines: Cell biology
                Keywords: rapamycin,senescence,geroconversion,gerosuppressants,mtor
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: rapamycin, senescence, geroconversion, gerosuppressants, mtor

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