Cellular senescence is a complex stress response that leads to an irreversible state of cell growth arrest. Senescence may be induced by various stimuli such as telomere shortening, DNA damage or oncogenic insult, among others. Senescent cells are metabolically highly active, producing a wealth of cytokines and chemokines that, depending on the context, may have a beneficial or deleterious effect on the organism. Senescence is considered a tightly regulated stress response that is largely governed by the p53/p21 and p16/Rb pathways. Many molecules have been identified as regulators of these two networks, such as transcription factors, chromatin modifiers and non-coding RNAs. The expression level of several long non-coding RNAs is affected during different types of senescence; however, which of these are important for the biological function remains poorly understood. Here we review our current knowledge of the mechanistic roles of lncRNAs affecting the main senescence pathways, and discuss the importance of identifying new regulators.
Cellular senescence is an irreversible state of cell growth arrest, which can be induced by different stimuli such as telomere shortening, oncogenic stress or DNA damage among others. Long non-coding RNAs (lncRNAs) have recently emerged as regulators of this process and we review here the current knowledge of the impact of, and the molecular mechanisms by which lncRNAs modulate senescence.