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Aging and disease    2017, Vol. 8 Issue (2) : 149-161     DOI: 10.14336/AD.2016.0810
Review |
Shining the Light on Senescence Associated LncRNAs
Ghanam A.R.1,2, Xu Qianlan1, Ke Shengwei1, Azhar Muhammad1, Cheng Qingyu1, Song Xiaoyuan1,*
1CAS Key Laboratory of Brain Function and Disease, CAS Center for Excellence in Molecular Cell Science, Collaborative Innovation Center of Chemistry for Life Sciences, School of Life Sciences, University of Science and Technology of China, Hefei 230027, China.
2Collage of Veterinary Medicine, Suez Canal University, Ismailia 41522, Egypt
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Cellular senescence can be described as a complex stress response that leads to irreversible cell cycle arrest. This process was originally described as an event that primary cells go through after many passages of cells during cell culture. More recently, cellular senescence is viewed as a programmed process by which the cell displays a senescence phenotype when exposed to a variety of stresses. Cellular senescence has been implicated in tumor suppression and aging such that senescence may contribute to both tumor progression and normal tissue repair. Here, we review different forms of cellular senescence, as well as current biomarkers used to identify senescent cells in vitro and in vivo. Additionally, we highlight the role of senescence-associated long noncoding RNAs (lncRNAs).

Keywords cellular senescence      lncRNAs      biomarkers     
Corresponding Authors: Song Xiaoyuan   
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These authors contributed equally to this work

Issue Date: 01 April 2017
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Ghanam A.R.
Xu Qianlan
Ke Shengwei
Azhar Muhammad
Cheng Qingyu
Song Xiaoyuan
Cite this article:   
Ghanam A.R.,Xu Qianlan,Ke Shengwei, et al. Shining the Light on Senescence Associated LncRNAs[J]. Aging and disease, 2017, 8(2): 149-161.
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Figure 1.  Timeline of pivotal steps in the study of senescence.
LncRNARole is senescenceCell cycle effectCitation
MALAT 1Inhibit senescence, promote cell divisionG0[85]
Gadd7Binds TDP-43, lowers Cdk6 mRNAG1/S[86]
MEG3Upregulates p53, blocks apoptosisN/A[87]
7SLInhibits senescence, suppresses p53G1, G2, S[88]
eRNAsp53-regulated, induce cellular senescenceG1[78]
UCA1Inhibits senescence, inhibits senescence cdki p27G1[89]
SRAInhibits senescence cdki p21, p27G2, M[90]
ANRILPrevents expression of p15 and p16N/A[69]
Kcnq 1OT1Cell division and DNA methylationN/A[48]
NcRNACCND1Inhibits transcription of CCND1 geneG1,S[91, 92]
HOTAIRScaffold for MEX3 and DZIP3 E3 ubiquitin LigaseG2, G1[44, 93]
TERRAEnhance mobility of shelterin proteins to keep
Telomere stability
AsncmtRNA2Up regulated in replicative senescenceN/A[95]
Table 1  LncRNAs affecting molecular traits in cell cycle of cellular senescence
Figure 2.  A photograph of the brain aging with time, telomere shortening, senescent cells or depletion of adult neural stem cells. Do we think we are able to keep our brain green in spite of time passing? Are we only able to delay the onset of our brain autumn and if we succeed in delaying it, will our life span be increased or only cellular function (healthiness) be improved during our limited lifespan?
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