IMR Press / FBL / Volume 17 / Issue 7 / DOI: 10.2741/4074

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Senescence; an endogenous anticancer mechanism
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1 Laboratory of Cellular Signaling and Plasticity, Department of Biophysics and Center of Biotechnology, Federal University of Rio Grande do Sul, Av. Bento Goncalves, 9500, Porto Alegre, Brazil
2 Institute of Biotechnology, University of Caxias do Sul, Rua Francisco Getulio Vargas 1130, Caxias do Sul, Brazil
3 Laboratory of Molecular Radiobiology, Department of Molecular Biology and Biotechnology, Federal University of Rio Grande do Sul, Av. Bento Goncalves, 9500, Porto Alegre, Brazil
Front. Biosci. (Landmark Ed) 2012, 17(7), 2616–2643;
Published: 1 June 2012

Pre-malignant tumor cells enter a state of irreversible cell cycle arrest termed senescence (cellular senescence; CS). CS is a part of the aging program and involves multiple signaling cascades and transduction mechanisms. In general, senescence can be divided into replicative senescence and premature senescence. Replicative senescence (replicative CS) has been described for all metabolically active cells that undergo a spontaneous decline in growth rate. Notably, ectopic expression of telomerase holoenzyme (hTert) can prevent replicative CS. In cancer cells, premature senescence induced by oncogenes, named oncogene-induced senescence (oncogene induced CS; OIS), play an important role in preventing the development of cancer. Oncogene induced CS can be promoted by the loss of tumor suppressor genes, such as PTEN. Additionally, other interesting mechanisms, like selective microRNA expression, epigenetic modifications, or even stress conditions, are also able to activate the senescence program. Here, we will critically review the literature on the role of senescence in preventing the development of cancer and discuss the potential of senescence modulation for generating new molecular tools that could be explored as anticancer treatments.

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