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Transcriptional Activation of the Telomerase hTERT Gene by Human Papillomavirus Type 16 E6 Oncoprotein
Abstract
The E6 and E7 oncogenes of human papillomavirus type 16 (HPV-16) are sufficient for the immortalization of human genital keratinocytes in vitro. The products of these viral genes associate with p53 and pRb tumor suppressor proteins, respectively, and interfere with their normal growth-regulatory functions. The HPV-16 E6 protein has also been shown to increase the telomerase enzyme activity in primary epithelial cells by an unknown mechanism. We report here that a study using reverse transcription-PCR and RNase protection assays in transduced primary human foreskin keratinocytes (HFKs) shows that the E6 gene (but not the E7 gene) increases telomerase hTERT gene transcription coordinately with E6-induced telomerase activity. In these same cells, the E6 gene induces a 6.5-fold increase in the activity of a 1,165-bp 5′ promoter/regulatory region of the hTERT gene, and this induction is attributable to a minimal 251-bp sequence (−211 to +40). Furthermore, there is a 35-bp region (+5 to +40) within this minimal E6-responsive promoter that is responsible for 60% of E6 activity. Although the minimal hTERT promoter contains Myc-responsive E-box elements and recent studies have suggested a role for Myc protein in hTERT transcriptional control, we found no alterations in the abundance of either c-Myc or c-Mad in E6-transduced HFKs, suggesting that there are other or additional transcription factors critical for regulating hTERT expression.
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“We have, however, determined that the promoter region including the proximal E box is important for E6-mediated hTERT induction (Gewin and Galloway 2001; Veldman et al. 2001).”
From Identification of a novel telomerase repressor that interacts with the human papillomavirus type-16 E6/E6-AP complex (2004) · cites this paper as Veldman et al. 2001
In the citing paper
“Although cMyc levels do not appear to change dramatically on E6 expression (Gewin and Galloway 2001; Veldman et al. 2001), two groups have recently found by chromatin immunoprecipitation that c-Myc is bound to the hTERT promoter in E6-expressing cells (Baege et al. 2002; Veldman et al. 2003).”
From Identification of a novel telomerase repressor that interacts with the human papillomavirus type-16 E6/E6-AP complex (2004) · cites this paper as Veldman et al. 2001
In the citing paper
“Although c-Myc is able to bind the E boxes in the hTERT promoter and can induce hTERT expression in many cell types (Wang et al. 1998; Greenberg et al. 1999; Wu et al. 1999), we and others have found no correlation between c-Myc expression and the ability of E6 to induce hTERT (Gewin and Galloway 2001; Oh et al. 2001; Veldman et al. 2001).”
From Identification of a novel telomerase repressor that interacts with the human papillomavirus type-16 E6/E6-AP complex (2004) · cites this paper as Veldman et al. 2001
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Cites
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“Using a modified TRAP assay (17, 35), telomerase activity was detected in HFKs expressing E6 alone or E6 plus E7 but not in HFKs expressing E7 alone.”
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Metadata
- Authors
- Veldman, T., Horikawa, I., Barrett, J. C., & Schlegel, R.
- Affiliations
- <!--label omitted: 1-->Departments of Pathology and Oncology, Georgetown University Medical School, Washington, D.C. 20007,1 and
- <!--label omitted: 2-->Laboratory of Biosystems and Cancer, Cancer and Aging Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 208922
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2001-05
- Volume
- 75
- Issue
- 9
- Pages
- 4467-4472
- ISSN
- 0022-538X
- 1098-5514
- Cited by
- 237
- References
- 8
- Language
- en
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