Document Detail

Tumor cell redox state and mitochondria at the center of the non-canonical activity of telomerase reverse transcriptase.
MedLine Citation:
PMID:  19995569     Owner:  NLM     Status:  MEDLINE    
Telomerase (hTERT) activation in cancer cells is an invariable finding resulting in the maintenance of telomere lengths and enhanced replicative capacity. Therefore a variety of therapeutic approaches are being investigated to target hTERT, such as hTERT-promoter driven expression of apoptosis inducing genes, inhibiting telomeric RNA (hTR), and anti-sense or siRNA mediated gene silencing. Whereas, the conventional oncogenic role of hTERT has been linked to its ability to induce replicative senescence and immortalization, evidence is accumulating to support non-canonical activity of hTERT in cancer cells. To that end, hTERT has been implicated in redox-mediated events and its expression has been shown to impact cellular redox status via the recruitment of the mitochondria, a critical intracellular source of reactive oxygen species (ROS). Further evidence in support of the role of mitochondria in hTERT biology comes from findings demonstrating localization of hTERT to the mitochondria, and the ability of hTERT inhibitors to induce mitochondrial-dependent apoptosis in target cells. Here we review the emerging evidence to support the involvement of the mitochondria and intracellular ROS as critical mediators of the non-canonical functions/activity of hTERT with potential implications for its therapeutic targeting in cancer cells.
Inthrani Raja Indran; Manoor Prakash Hande; Shazib Pervaiz
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Publication Detail:
Type:  Journal Article; Review     Date:  2009-12-06
Journal Detail:
Title:  Molecular aspects of medicine     Volume:  31     ISSN:  1872-9452     ISO Abbreviation:  Mol. Aspects Med.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-03-10     Completed Date:  2010-06-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7603128     Medline TA:  Mol Aspects Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  21-8     Citation Subset:  IM    
Copyright Information:
2009 Elsevier Ltd. All rights reserved.
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
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MeSH Terms
Mitochondria / enzymology*,  metabolism
Neoplasms / enzymology*,  metabolism,  pathology
Reactive Oxygen Species / metabolism
Telomerase / metabolism*
Reg. No./Substance:
0/Reactive Oxygen Species; EC

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