Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.mam.2009.12.001
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dc.titleTumor cell redox state and mitochondria at the center of the non-canonical activity of telomerase reverse transcriptase
dc.contributor.authorIndran, I.R.
dc.contributor.authorHande, M.P.
dc.contributor.authorPervaiz, S.
dc.date.accessioned2011-07-27T06:40:02Z
dc.date.available2011-07-27T06:40:02Z
dc.date.issued2010
dc.identifier.citationIndran, I.R., Hande, M.P., Pervaiz, S. (2010). Tumor cell redox state and mitochondria at the center of the non-canonical activity of telomerase reverse transcriptase. Molecular Aspects of Medicine 31 (1) : 21-28. ScholarBank@NUS Repository. https://doi.org/10.1016/j.mam.2009.12.001
dc.identifier.issn00982997
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/25025
dc.description.abstractTelomerase (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. © 2009 Elsevier Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.mam.2009.12.001
dc.sourceScopus
dc.subjectApoptosis
dc.subjecthTERT
dc.subjectMitochondria
dc.subjectROS
dc.subjectSenescence
dc.typeReview
dc.contributor.departmentPHYSIOLOGY
dc.description.doi10.1016/j.mam.2009.12.001
dc.description.sourcetitleMolecular Aspects of Medicine
dc.description.volume31
dc.description.issue1
dc.description.page21-28
dc.identifier.isiut000276729700002
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