Viruses 2017, 9(7), 180; https://doi.org/10.3390/v9070180
Telomerase Induction in HPV Infection and Oncogenesis
1
Center for Global Infectious Disease Research, Seattle Children’s Research Institute, Seattle, WA 98101, USA
2
Department of Pediatrics, Division of Adolescent Medicine, University of Washington, Seattle, WA 98195, USA
Academic Editors: Alison A. McBride and Karl Munger
Received: 15 June 2017 / Revised: 5 July 2017 / Accepted: 7 July 2017 / Published: 10 July 2017
(This article belongs to the Special Issue Expert Views on HPV Infection)
Abstract
Telomerase extends the repetitive DNA at the ends of linear chromosomes, and it is normally active in stem cells. When expressed in somatic diploid cells, it can lead to cellular immortalization. Human papillomaviruses (HPVs) are associated with and high-risk for cancer activate telomerase through the catalytic subunit of telomerase, human telomerase reverse transcriptase (hTERT). The expression of hTERT is affected by both high-risk HPVs, E6 and E7. Seminal studies over the last two decades have identified the transcriptional, epigenetic, and post-transcriptional roles high-risk E6 and E7 have in telomerase induction. This review will summarize these findings during infection and highlight the importance of telomerase activation as an oncogenic pathway in HPV-associated cancer development and progression. View Full-TextKeywords:
human papillomavirus; papillomaviruses; oncogenic virus; cancer; HPV E6; HPV E7; hTERT; telomerase
▼
Figures
Figure 1
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
Share & Cite This Article
MDPI and ACS Style
Katzenellenbogen, R. Telomerase Induction in HPV Infection and Oncogenesis. Viruses 2017, 9, 180.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.