ArticleVirus genes2015
Integration of the full-length HPV16 genome in cervical cancer and Caski and Siha cell lines and the possible ways of HPV integration.
Article in Virus genes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Hsa_circ_0000231 activates the MAPK pathway via IGF2BP2-mediated CACNA1H mRNA stabilization to promote cervical cancer progression.Discover oncology · 2026Article
- An amplicon-based approach for full-genome characterization of HPV16.Microbiology spectrum · 2025Article
- A Combination of Flavonoids Suppresses Cell Proliferation and the E6 Oncogenic Pathway in Human Papillomavirus-Transformed Cells.Pathogens (Basel, Switzerland) · 2025Article
- Circulating cell-free HPV DNA is a strong marker for disease severity in cervical cancer.Molecular oncology · 2024Article
- Review
- CDK6 increases glycolysis and suppresses autophagy by mTORC1-HK2 pathway activation in cervical cancer cells.Cell cycle (Georgetown, Tex.) · 2022Article
- Analysis of HPV Integrations in Mexican Pre-Tumoral Cervical Lesions Reveal Centromere-Enriched Breakpoints and Abundant Unspecific HPV Regions.International journal of molecular sciences · 2021Article
- Human papilloma virus (HPV) integration signature in Cervical Cancer: identification of MACROD2 gene as HPV hot spot integration site.British journal of cancer · 2021Article
- Whole Genome Assembly of Human Papillomavirus by Nanopore Long-Read Sequencing.Frontiers in genetics · 2021Article
- Human Papillomavirus E7 Oncoprotein Subverts Host Innate Immunity via SUV39H1-Mediated Epigenetic Silencing of Immune Sensor Genes.Journal of virology · 2020Article
- CRISPR-typing PCR (ctPCR), a new Cas9-based DNA detection method.Scientific reports · 2018Article
- Oxidative stress in female cancers.Oncotarget · 2018Review
- Integration sites of human papillomavirus 18 in esophageal cancer samples.Oncology letters · 2018Article
- Article
- Inhibition of MMP-9 expression by ritonavir or saquinavir is associated with inactivation of the AKT/Fra-1 pathway in cervical intraepithelial neoplasia cells.Oncology letters · 2017Article
- Novel insights into epigenetic drivers of oropharyngeal squamous cell carcinoma: role of HPV and lifestyle factors.Clinical epigenetics · 2017Review
- Analysis of E2 gene integrity in HPV16 and HPV58 viruses isolated from women with cervical pathology.Memorias do Instituto Oswaldo Cruz · 2016Article
- The correlation between HLA-DRB1 and HLA-DQB1 gene polymorphisms and cytokines in HPV16 infected women with advanced cervical cancer.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integration of high-risk human papillomavirus (HPV) into the host genome is a key event for cervical carcinogenesis. Different methods have been used to explore the physical states of the HPV genome to reveal the mechanisms for malignant transformation of the infected cells. Consensus has been reached that, although variable portions of the HPV genome are deleted in the integrated HPV sequences, common disruption of the viral E2 gene has been demonstrated in different studies. The head-to-tail concatemers of the full-length HPV16 genome is another typical integration pattern of HPV16, typically found in Caski cell lines, but its prevalence in cervical cancer has never been tested. Here, by introducing a modified PCR, we identified this head-to-tail concatemers of full-length HPV genomes in advanced cervical cancer with HPV16 single positive. Our results show that more than half of the cases contain this integrated head-to-tail concatemers of full-length HPV16 genomes. Further studies in two cervical cell lines, Caski cells and Siha cells, revealed a correlation between the prevalence of the spliced variants of integrated HPV16 sequences and the full-length transcription of the integrated head-to-tail concatemers of the full-length HPV16 genome. Based on these results, we propose that HPV16 integrated into host cells by two mechanisms: one mechanism is shared by other DNA virus and cause integration of the head-to-tail concatemers of the viral genome; another is related to the reverse transcription process, which the integrated HPV sequence is generated by the reverse transcription of the viral mRNA.
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