ArticlebioRxiv : the preprint server for biology2025
Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Molecular, immunological and oncogenic mechanisms of cervical cancer mediated by HPV/HIV co-infection, clinical implication and management.Infectious agents and cancer · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-risk human papillomavirus (HPV) infections are the etiology of approximately 5% of all cancers worldwide, including cervical, anal, and oropharyngeal malignancies. HPV E6 is a multifunctional oncoprotein that drives tumorigenesis and is best known for bridging the ubiquitin ligase E6AP (UBE3A) and p53 into a complex that leads to proteasome mediated destruction of p53. We developed small molecule inhibitors that covalently bind to cysteine-51 (Cys-51) in HPV16 E6. In HPV16-positive cancer cells, these compounds increase p53 protein levels and activate p53-dependent transcriptional programs associated with apoptosis and senescence, resulting in reduced tumor cell viability.
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Registered trials
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