期刊
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK
卷 33, 期 7, 页码 1041-1051出版社
WILEY
DOI: 10.1002/hed.21579
关键词
TERT; ALT; telomere; ribosome biogenesis; oral carcinogenesis
资金
- NIH [DE018416, DE015856]
- University of Pennsylvania Research Foundation
- University of Pennsylvania's Abramson Cancer Center
- Pennsylvania Department of Health
Background. Dyskerin, which is an important component of the telomerase complex and is needed for normal telomerase activity, is frequently overexpressed in neoplasia. Dyskerin also plays an essential role in ribosome biogenesis. Because protein synthesis increases during tumorigenesis, this led us to hypothesize that dyskerin expression would be upregulated independently of the cell immortalization mechanism. Methods. Dyskerin and telomerase reverse transcriptase (TERT) expression were examined in oral squamous cell carcinomas (OSCC) and patient-matched controls, as well as in a panel of telomerase-positive and telomerase-negative cells. Antisense inhibition of TERT was used to test the effects of downregulation of telomerase on dyskerin expression. Results. Dyskerin was frequently overexpressed in OSCC and in immortalized and transformed keratinocytes relative to primary cells, independently of TERT and telomerase activity. Instead, dyskerin expression strongly correlated with cell proliferation rates. Conclusions. The role of dyskerin in tumorigenesis does not correlate with its function within the telomerase complex. (C) 2010 Wiley Periodicals, Inc. Head Neck 33: 1041-1051, 2011
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