ArticleVirology2008
HPV E7 contributes to the telomerase activity of immortalized and tumorigenic cells and augments E6-induced hTERT promoter function.
Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 89 citations in OpenAlex.
- HPV18E6 and CDK5 virus-host interaction is a prospective therapeutic target for HPV-positive cervical cancer.Tumour virus research · 2026Article
- Comparative Analysis Reveals Recurrent Molecular Alterations in Low-Risk Human Papillomavirus 6 and Human Papillomavirus 11-Associated Squamous Cell Carcinoma of the Uterine Cervix and Vulva.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2025Article
- Canonical and non-canonical functions of the non-coding RNA component (TERC) of telomerase complex.Cell & bioscience · 2025Review
- Rapid and Sensitive Digital Droplet PCR Assays for Detecting HPV16 DNA in Liquid Biopsies.Journal of medical virology · 2025Article
- Dysregulated microRNA Expression Relevant toLife (Basel, Switzerland) · 2023Article
- The Value of CXCL1, CXCL2, CXCL3, and CXCL8 as Potential Prognosis Markers in Cervical Cancer: Evidence of E6/E7 from HPV16 and 18 in Chemokines Regulation.Biomedicines · 2023Article
- Identification of HPV oncogene and host cell differentiation associated cellular heterogeneity in cervical cancer via single-cell transcriptomic analysis.bioRxiv : the preprint server for biology · 2023Article
- Immortalization Reversibility in the Context of Cell Therapy Biosafety.International journal of molecular sciences · 2023Review
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- Small-molecule eRF3a degraders rescue CFTR nonsense mutations by promoting premature termination codon readthrough.The Journal of clinical investigation · 2022Article
- Do or Die: HPV E5, E6 and E7 in Cell Death Evasion.Pathogens (Basel, Switzerland) · 2022Review
- Oncogenic Viruses as Entropic Drivers of Cancer Evolution.Frontiers in virology (Lausanne, Switzerland) · 2021Article
- Negative Prognostic Implication ofIndian journal of surgical oncology · 2021Article
- Establishment of an Immortalized Endometriotic Stromal Cell Line from Human Ovarian Endometrioma.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Conditional reprogramming: next generation cell culture.Acta pharmaceutica Sinica. B · 2020Review
- Human Papillomavirus 58 E7 T20I/G63S Variant Isolated from an East Asian Population Possesses High Oncogenicity.Journal of virology · 2020Article
- Telomere length in cervical exfoliated cells, interaction with HPV genotype, and cervical cancer occurrence among high-risk HPV-positive women.Cancer medicine · 2019Article
- Lymphocyte telomere length predicts clinical outcomes of HPV-positive oropharyngeal cancer patients after definitive radiotherapy.Carcinogenesis · 2019Article
- Δ133p53α, a natural p53 isoform, contributes to conditional reprogramming and long-term proliferation of primary epithelial cells.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The E6 and E7 proteins of high-risk HPVs are both required for the immortalization of primary human keratinocytes and the maintenance of the malignant phenotype of HPV-positive cancer cell lines. Our previous studies have shown that E6 protein binds Myc protein and that both E6 and Myc associate with and cooperatively activate the hTERT promoter, thereby increasing cellular telomerase activity. In this study, we evaluated the role of E7 in the maintenance and activation of telomerase in immortalized and tumorigenic cells. siRNA knockdown of either E6 or E7 (or both) in HPV-immortalized cells or an HPV-positive cancer cell line reduced hTERT transcription and telomerase activity. Since telomerase was inhibited by E7 siRNA in cells that independently expressed the E6 and E7 genes, our results reveal an independent role for E7 in the maintenance of telomerase activity. However, E7 alone was insufficient to increase endogenous hTERT mRNA or telomerase activity, although it significantly augmented E6-induced hTERT transcription and telomerase activity. To further explore this apparent E7-induced promoter augmentation, we analyzed an exogenous hTERT core promoter in transduced keratinocytes. E7 alone induced the wt hTERT promoter and augmented E6-induced hTERT promoter activity. Mutation of the E2F site in the hTERT promoter abrogated the ability of E7 to induce the hTERT promoter or to enhance the ability of E6 to induce the promoter. Correspondingly, keratinocytes expressing E6 and a mutant E7 (defective for binding pRb pocket proteins) showed lower telomerase activity than cells expressing wt E6 and wt E7. Thus, HPV E7 plays a role in the maintenance of telomerase activity in stable cell lines and augments acute, E6-induced hTERT promoter activity.
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