Cellular Senescence is a Common Characteristic Shared by Preneoplasic and Osteo-Arthritic Tissue
Jean-Marc Brondello*, 1, Didier Philipot1, Farida Djouad1, Christian Jorgensen1, 2, 3, Danièle Noël1
Identifiers and Pagination:Year: 2010
First Page: 10
Last Page: 14
Publisher ID: TORJ-4-10
Article History:Received Date: 6/12/2009
Revision Received Date: 6/1/2010
Acceptance Date: 18/1/2010
Electronic publication date: 11/2/2010
Collection year: 2010
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
This study aims at highlighting the common signature between cartilaginous tissue in osteoarthritis (OA) and preneoplasic tissues preceding neoplasia and tumour formation and, second, focusing on the molecular mechanisms at the aetiology of both pathologies.
Because age is the highest risk factor common for both OA and cancer development, it is tempting to compare the molecular mechanisms occurring at the onset of OA and preneoplasic lesions. Indeed, cellular senescence seems to be a common characteristic. Cellular senescence represents a natural barrier to suppress the unscheduled proliferation of damaged cells acting as a strong tumour suppressor pathway and in OA, it also occurs prematurely in chondrocytes. In this study, we review a number of molecular factors associated with the senescent phenotype.
Whereas accumulation of senescent cells in preneoplasic-like lesions leads to tissue degeneration and potentially tumour development; in OA, senescent cells accumulate in a slowly proliferative tissue. This is likely contributing at reducing the risk of cell transformation.