期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 347, 期 3, 页码 774-780出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2006.06.172
关键词
telomerase; hTERT; cyclin D1; cell cycle; prostate cancer; DU-145; BPH-1
资金
- NIDDK NIH HHS [R01 DK060875] Funding Source: Medline
Cells require a mechanism to maintain telomere stability in order to overcome replicative senescence and telomerase catalyzes the synthesis and extension of telomeric DNA, therefore, be a rate-limiting step in cellular immortality and oncogenesis. However, some studies have raised questions about whether the stabilization of chromosome ends entirely explains the ability of telomerase to promote tumorigenesis. To elucidate non-canonical functions of human telomerase reverse transcriptase (hTERT), we used loss-of-function and gain-of-function studies. We demonstrated that hTERT shRNA down-regulated and hTERT overexpression up-regulated the expression and transcriptional activity of a key cell cycle regulator, cyclin D1, in human prostate epithelial cell lines, DU-145 and BPH-1. Based on these observations, we propose that in addition to its well-defined function in telomere length regulation, hTERT has a novel role in the modulation of cyclin D1 expression. (c) 2006 Elsevier Inc. All rights reserved.
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