ArticleCancer letters2019
NFX1-123 is highly expressed in cervical cancer and increases growth and telomerase activity in HPV 16E6 expressing cells.
Article in Cancer letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- NFX1-123 is required for keratinocyte differentiation and HPV 16 DNA maintenance in early and persistent infection models.Journal of virology · 2026Article
- Novel examples of NMD escape through alternative intronic polyadenylation.NAR genomics and bioinformatics · 2026Article
- Proliferative proteome induced by HPV 16E6 and NFX1-123 partnership in longitudinal keratinocyte cultures.Journal of virology · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Roles of human papillomavirus in cancers: oncogenic mechanisms and clinical use.Signal transduction and targeted therapy · 2025Review
- The microbial conductor of cancer hallmarks: intratumoral microbiome as a multidimensional oncogenic modulator.Frontiers in microbiology · 2025Review
- Review
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
- NFX1-123: A potential therapeutic target in cervical cancer.Journal of medical virology · 2023Article
- The Molecular Interplay between Human Oncoviruses and Telomerase in Cancer Development.Cancers · 2022Review
- Review
- Review
- High expression of NFX1-123 in HPV positive head and neck squamous cell carcinomas.Head & neck · 2022Article
- Article
- Review
- Genes Regulated by HPV 16 E6 and High Expression of NFX1-123 in Cervical Cancers.OncoTargets and therapy · 2020Article
- CircAMOTL1 Promotes Tumorigenesis Through miR-526b/SIK2 Axis in Cervical Cancer.Frontiers in cell and developmental biology · 2020Article
- HPV type 16 E6 and NFX1-123 augment JNK signaling to mediate keratinocyte differentiation and L1 expression.Virology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
A significant contributor to women's cancer mortality worldwide is cervical cancer, which is caused by high-risk human papillomavirus (HR HPV). The two viral oncoproteins of HR HPV, E6 and E7, partner with host cell proteins to target oncogenic proteins and pathways. Previously, we have shown HR HPV type 16 E6 (16E6) interacts with the host protein NFX1-123 to target telomerase and cellular immortalization, requiring NFX1-123 to fully upregulate telomerase activity. We now report that NFX1-123 is highly expressed in primary cervical cancers. In vitro, cells expressing 16E6 and overexpressing NFX1-123 have extended active growth, decreased senescence marker staining, and more rapid cell cycling compared to 16E6 expressing cells with endogenous amounts of NFX1-123. These findings were associated with increased telomerase activity and augmented expression of its catalytic subunit, hTERT. In complement, HPV 16 positive cervical cancer cell lines with knocked down NFX1-123 had slowed growth and reduced hTERT over time. In cells that express HR HPV E6, greater expression of NFX1-123 can modify active cellular growth and augment hTERT expression and telomerase activity over time, potentially supporting the initiation and progression of HPV-associated cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.