Document Detail

Rapamycin decelerates cellular senescence.
MedLine Citation:
PMID:  19471117     Owner:  NLM     Status:  MEDLINE    
When the cell cycle is arrested but cellular growth is not, then cells senesce, permanently losing proliferative potential. Here we demonstrated that the duration of cell cycle arrest determines a progressive loss of proliferative capacity. In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative potential caused by ectopic p21, p16 and sodium butyrate-induced p21. Thus, when the cell cycle was arrested by these factors in the presence of rapamycin, cells retained the capacity to resume proliferation, once p21, p16 or sodium butyrate were removed. While rapamycin prevented the permanent loss of proliferative potential in arrested cells, it did not force the arrested cells into proliferation. During cell cycle arrest, rapamycin transformed the irreversible arrest into a reversible condition. Our data demonstrate that senescence can be pharmacologically suppressed.
Zoya N Demidenko; Svetlana G Zubova; Elena I Bukreeva; Valery A Pospelov; Tatiana V Pospelova; Mikhail V Blagosklonny
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-06-01
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  8     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-06-01     Completed Date:  2009-08-14     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1888-95     Citation Subset:  IM    
Oncotarget, Albany, NY, USA.
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MeSH Terms
Butyrates / pharmacology
Cell Aging / drug effects*,  physiology
Cell Cycle / drug effects*,  physiology
Cell Line
Cell Line, Tumor
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Isopropyl Thiogalactoside / pharmacology
Neoplasm Proteins / metabolism
Protein Kinases / drug effects*,  metabolism
Sirolimus / pharmacology*
Grant Support
1 R41 EY018520-01/EY/NEI NIH HHS
Reg. No./Substance:
0/Butyrates; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Neoplasm Proteins; 0/P16 protein, human; 367-93-1/Isopropyl Thiogalactoside; 53123-88-9/Sirolimus; EC 2.7.-/Protein Kinases; EC 2.7.1.-/mTOR protein
Comment In:
Cell Cycle. 2009 Jun 15;8(12):1820-1   [PMID:  19471126 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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