AI Article Synopsis
- Cellular senescence serves as a protective mechanism against cancer by causing normal cells to stop dividing in response to stressors like DNA damage or telomere shortening.
- *It involves tumor suppressor pathways that must be deactivated for cancer cells to escape senescence and continue proliferating uncontrollably.
- *MicroRNAs play a crucial role in regulating cellular senescence signals and the expression of these miRNAs is influenced by the senescence response, especially in relation to cancer and age-related diseases.
Article Abstract
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.
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| http://dx.doi.org/10.1016/bs.ircmb.2017.04.001 | DOI Listing |
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