PMID- 27558094
OWN - NLM
STAT- MEDLINE
DCOM- 20170308
LR  - 20211204
IS  - 1573-4978 (Electronic)
IS  - 0301-4851 (Linking)
VI  - 43
IP  - 11
DP  - 2016 Nov
TI  - The cell fate: senescence or quiescence.
PG  - 1213-1220
AB  - Senescence and quiescence are frequently used as interchangeable terms in the 
      literature unwittingly. Despite the fact that common molecules play role in 
      decision of cell cycle arrest, senescent and quiescent cells have some 
      distinctive phenotypes at both molecular and morphological levels. Thus, in this 
      review we summarized the features of senescence and quiescence with respect to 
      visual characteristics and prominent key molecules. A PubMed research was 
      conducted for the key words; "senescence", "quiescence" and "cell cycle arrest". 
      The results which are related to cell cycle control were selected. The selection 
      criteria of the target articles used for this review included also key cell cycle 
      molecules such as p53, pRB, p21, p16, mTOR, p27, etc. The results were not 
      evaluated statistically. The mechanistic target of rapamycin (mTOR) has been 
      claimed to be key molecule in switching on/off senescence/quiescence. 
      Specifically, although maximal p53 activation blocks mTOR and causes quiescence, 
      partial p53 activation sustains mTOR activity and causes senescence subsequently. 
      In broader perspective, quiescence occurs due to lack of nutrition and growth 
      factors whereas senescence takes place due to aging and serious DNA damages. 
      Contrary to quiescence, senescence is a degenerative process ensuing a certain 
      cell death. We highlighted several differences between senescence and quiescence 
      and their key molecules in this review. Whereas quiescence (cell cycle arrest) is 
      only one half of the senescence, the other half is growth stimulation which 
      causes actual senescence phenotype.
FAU - Terzi, Menderes Yusuf
AU  - Terzi MY
AD  - Department of Medical Biology, Faculty of Medicine, Mustafa Kemal University, 
      Serinyol Campus, 31034, Antakya, Hatay, Turkey.
FAU - Izmirli, Muzeyyen
AU  - Izmirli M
AD  - Department of Medical Biology, Faculty of Medicine, Mustafa Kemal University, 
      Serinyol Campus, 31034, Antakya, Hatay, Turkey. muzeyyenizmirli@gmail.com.
FAU - Gogebakan, Bulent
AU  - Gogebakan B
AD  - Department of Medical Biology, Faculty of Medicine, Mustafa Kemal University, 
      Serinyol Campus, 31034, Antakya, Hatay, Turkey.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20160824
PL  - Netherlands
TA  - Mol Biol Rep
JT  - Molecular biology reports
JID - 0403234
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - *Cell Cycle Checkpoints
MH  - *Cellular Senescence
MH  - Gene Expression Regulation
MH  - Humans
MH  - Signal Transduction
MH  - Stem Cells/*cytology
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
OTO - NOTNLM
OT  - Quiescence
OT  - Senescence
OT  - mTOR
OT  - p53
EDAT- 2016/10/19 06:00
MHDA- 2017/03/09 06:00
CRDT- 2016/08/26 06:00
PHST- 2016/04/23 00:00 [received]
PHST- 2016/08/16 00:00 [accepted]
PHST- 2016/10/19 06:00 [pubmed]
PHST- 2017/03/09 06:00 [medline]
PHST- 2016/08/26 06:00 [entrez]
AID - 10.1007/s11033-016-4065-0 [pii]
AID - 10.1007/s11033-016-4065-0 [doi]
PST - ppublish
SO  - Mol Biol Rep. 2016 Nov;43(11):1213-1220. doi: 10.1007/s11033-016-4065-0. Epub 
      2016 Aug 24.