Document Detail


Survivin and escaping in therapy-induced cellular senescence.
MedLine Citation:
PMID:  20503268     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Therapy-induced accelerated cellular senescence (ACS) is a reversible tumor response to chemotherapy that is likely detrimental to the overall therapeutic efficacy of cancer treatment. To further understand the mechanism by which cancer cells can escape the sustained cell cycle arrest in ACS, we established a tissue culture model, in which the p53-null NCI-H1299 cells can be induced into senescence by an abbreviated exposure to a chemotherapeutic agent. Previously, we have reported that senescent cells overexpress Cdc2/Cdk1 when they bypassed the prolonged arrest and their viability is dependent on Cdc2/Cdk1 kinase activity. In our study, we show that human survivin is the immediate downstream effector of the Cdc2/Cdk1 mediated survival signal. Survivin cooperates with Cdc2/Cdk1 to inhibit apoptosis following chemotherapy and promote senescence escape. Using HIV-1 TAT peptides to disrupt survivin phosphorylation by Cdc2/Cdk1, we also found that phosphorylated survivin is necessary both for the escape of senescent cells and for maintenance of subsequent viability after bypassing senescence. These results further propose survivin as an important determinant of senescence reversibility and as a putative molecular target to enforce cell death in ACS.
Authors:
Qin Wang; Peter C Wu; Rachel S Roberson; Belinda V Luk; Iana Ivanova; Elizabeth Chu; Daniel Y Wu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-05-25
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  128     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-01-31     Completed Date:  2011-04-04     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1546-58     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 UICC.
Affiliation:
Seattle Institute for Biomedical and Clinical Research, VA Puget Sound Health Care System, Seattle, Washington. proteinss@hotmail.com
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MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents / pharmacology
Apoptosis
CDC2 Protein Kinase / metabolism
Cell Aging*
Cell Line, Tumor
Cyclin B / metabolism
Gene Products, tat / metabolism
Humans
Microtubule-Associated Proteins / metabolism*
Oligonucleotides, Antisense / chemistry
Phosphorylation
RNA, Small Interfering / metabolism
Grant Support
ID/Acronym/Agency:
R01 CA113892-01A1/CA/NCI NIH HHS; R01-CA113892-01/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/BIRC5 protein, human; 0/CDC2 protein, human; 0/Cyclin B; 0/Gene Products, tat; 0/Microtubule-Associated Proteins; 0/Oligonucleotides, Antisense; 0/RNA, Small Interfering; EC 2.7.11.22/CDC2 Protein Kinase

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


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