Molecular Regulation of Cellular Senescence by MicroRNAs: Implications in Cancer and Age-Related Diseases.
Author: Neault M1, Couteau F2, Bonneau É3, De Guire V4, Mallette FA5
Affiliation:
1Chromatin Structure and Cellular Senescence Research Unit, Maisonneuve-Rosemont Hospital Research Centre, Montréal, QC, Canada; Université de Montréal, Montréal, QC, Canada.
2Chromatin Structure and Cellular Senescence Research Unit, Maisonneuve-Rosemont Hospital Research Centre, Montréal, QC, Canada.
3Maisonneuve-Rosemont Hospital, Montréal, QC, Canada.
4Université de Montréal, Montréal, QC, Canada; Maisonneuve-Rosemont Hospital, Montréal, QC, Canada.
5Chromatin Structure and Cellular Senescence Research Unit, Maisonneuve-Rosemont Hospital Research Centre, Montréal, QC, Canada; Université de Montréal, Montréal, QC, Canada. Electronic address: fa.mallette@umontreal.ca.
Conference/Journal: Int Rev Cell Mol Biol.
Date published: 2017
Other:
Volume ID: 334 , Pages: 27-98 , Special Notes: doi: 10.1016/bs.ircmb.2017.04.001. Epub 2017 May 18. , Word Count: 154
Cellular senescence is a tumor suppressor response that acts as a barrier to cancer development and progression. In normal cells, diverse stimuli, including excessive mitogenic signaling, DNA damage or telomere shortening, trigger a senescence response characterized by stable growth arrest. Cellular senescence is orchestrated by tumor suppressor pathways, which have to be inactivated in order to impair the establishment of senescence and promote cancer. Consequently, by overcoming or bypassing this cellular response, cancer cells evade cell cycle checkpoint control leading to genomic instability and uncontrolled proliferation. MicroRNAs (MiRs) have emerged as essential factors contributing to or preventing cellular senescence. Here we detail the molecular mechanisms underlying the fine-tuning of cellular senescence signals by MiRs, and how the senescence response itself contributes to modulation of MiR expression, with a special focus on cancer and pathologies associated with aging.
© 2017 Elsevier Inc. All rights reserved.
KEYWORDS: Aging; Cancer; Cellular senescence; MiR; RB; p53
PMID: 28838541 DOI: 10.1016/bs.ircmb.2017.04.001
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