کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1995879 1541469 2010 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Tumor cell redox state and mitochondria at the center of the non-canonical activity of telomerase reverse transcriptase
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Tumor cell redox state and mitochondria at the center of the non-canonical activity of telomerase reverse transcriptase
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Aspects of Medicine - Volume 31, Issue 1, February 2010, Pages 21–28
نویسندگان
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