ArticleJournal of virology2007
Myc and human papillomavirus type 16 E7 genes cooperate to immortalize human keratinocytes.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- EZH2-Myc Hallmark in Oncovirus/Cytomegalovirus Infections and Cytomegalovirus' Resemblance to Oncoviruses.Cells · 2024Review
- Can prophylactic HPV vaccination reduce the recurrence of cervical lesions after surgery? Review and prospect.Infectious agents and cancer · 2023Review
- 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
- Novel canonical and non-canonical viral antigens extend current targets for immunotherapy of HPV-driven cervical cancer.iScience · 2023Article
- HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer.PLoS pathogens · 2023Article
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Human papillomavirus E6 and E7: What remains?Tumour virus research · 2021Review
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Modeling and Molecular Dynamics of the 3D Structure of the HPV16 E7 Protein and Its Variants.International journal of molecular sciences · 2021Article
- Conditionally Reprogrammed Human Normal Airway Epithelial Cells at ALI: A Physiological Model for Emerging Viruses.Virologica Sinica · 2020Review
- Conditional Reprogramming for Patient-Derived Cancer Models and Next-Generation Living Biobanks.Cells · 2019Review
- Human Papillomavirus E6 and E7: The Cervical Cancer Hallmarks and Targets for Therapy.Frontiers in microbiology · 2019Review
- A prospect of cell immortalization combined with matrix microenvironmental optimization strategy for tissue engineering and regeneration.Cell & bioscience · 2019Review
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
- Direct HPV E6/Myc interactions induce histone modifications, Pol II phosphorylation, and hTERT promoter activation.Oncotarget · 2017Article
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- ROCK inhibitor reduces Myc-induced apoptosis and mediates immortalization of human keratinocytes.Oncotarget · 2016Article
- TERT promoter hot spot mutations are frequent in Indian cervical and oral squamous cell carcinomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- E6AP in the brain: one protein, dual function, multiple diseases.Molecular neurobiology · 2014Article
- Evidences suggesting involvement of viruses in oral squamous cell carcinoma.Pathology research international · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The E6 protein of the oncogenic human papillomaviruses (HPVs), in combination with the E7 protein, is essential for the efficient immortalization of human foreskin keratinocytes (HFKs). Since we recently demonstrated that E6 activates the human telomerase reverse transcriptase (hTERT) promoter via a Myc-dependent mechanism, we speculated that overexpressed Myc might be able to substitute for E6 in cell immortalization. Myc (similar to E6) was unable to immortalize HFKs when transduced alone, despite inducing high levels of telomerase activity. However, when transduced with E7, Myc immortalized HFKs following a brief but detectable crisis period. In contrast to E6 + E7-immortalized cells, the Myc + E7-immortalized cells expressed high levels of p53 protein as well as two p53-regulated proteins, p21 and hdm-2. The increase in p21 and hdm-2 proteins correlated directly with their mRNA levels, suggesting transcriptional activation of the respective genes by the overexpressed p53 protein. Interestingly, a significant proportion of the p53 protein in the Myc + E7-immortalized cells was localized to the cytoplasm, potentially due to interactions with the overexpressed hdm-2 protein. Regardless, cell immortalization by the Myc + E7 genes occurred independently of p53 degradation. Since we have already observed high-efficiency cell immortalization with the hTERT + E7 or E6 mutant (p53 degradation-defective) + E7 genes (i.e., no crisis period) that proceeds in the presence of high levels of p53, we hypothesize that the crisis period in the Myc + E7 cells is due not to the levels of the p53 protein but rather to unique properties of the Myc protein. The common factor in cell immortalization by the three gene sets (E6 + E7, Myc + E7, and hTERT + E7 genes) is the induction of telomerase activity.
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Registered trials
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