ArticleJournal of virology2002
The human papillomavirus type 16 E5 protein impairs TRAIL- and FasL-mediated apoptosis in HaCaT cells by different mechanisms.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- The role of bevacizumab as an adjuvant to surgery in recurrent laryngeal papillomatosis: a systematic review of recurrence event outcomes.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Pooled it
- MicroRNA Dysregulation in HPV-Driven Cervical Cancer: A Review of Oncoprotein-Targeted Signaling Pathways.Life (Basel, Switzerland) · 2026Review
- Virus-mediated immunosuppression in head and neck cancer.Oncogene · 2025Review
- Review
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer.PLoS pathogens · 2023Article
- Review
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Molecular Mechanisms of HIV Protease Inhibitors Against HPV-Associated Cervical Cancer: Restoration ofFrontiers in molecular biosciences · 2022Review
- Therapeutic Effects of Natural Products on Cervical Cancer: Based on Inflammatory Pathways.Frontiers in pharmacology · 2022Review
- Virus against virus: strategies for using adenovirus vectors in the treatment of HPV-induced cervical cancer.Acta pharmacologica Sinica · 2021Review
- Cell death in head and neck cancer pathogenesis and treatment.Cell death & disease · 2021Review
- Glycogene expression profiles from a HaCaT cell line stably transfected with HPV16 E5 oncogene.Molecular medicine reports · 2020Article
- Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection.PLoS pathogens · 2020Article
- Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors.Biochemistry. Biokhimiia · 2020Review
- Put a cork in it: Plugging the M2 viral ion channel to sink influenza.Antiviral research · 2020Review
- Human Papillomaviruses and Epstein-Barr Virus Interactions in Colorectal Cancer: A Brief Review.Pathogens (Basel, Switzerland) · 2020Review
- HPV16 E5 Mediates Resistance to PD-L1 Blockade and Can Be Targeted with Rimantadine in Head and Neck Cancer.Cancer research · 2020Article
- Regulation of Autophagy in Cells Infected With Oncogenic Human Viruses and Its Impact on Cancer Development.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of the human papillomavirus type 16 (HPV-16) E5 protein on apoptosis was investigated by using the polyclonal HaCaT-cell lines stably transfected either with E5 (HaCaT/E5) or the empty vector (HaCaT/pMSG) as reference. Apoptosis was triggered either by Fas ligand (FasL) or by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and was monitored by detection of cleavage of procaspase-8 and procaspase-3, as well as their substrate poly(ADP-ribose) polymerase (PARP). In contrast to the HaCaT/pMSG control cells we found that apoptosis induced by either of the two ligands is strongly suppressed in the E5-expressing keratinocytes. Fas expression is reduced by about a factor of two in HaCaT/E5 cells, which could be part of the mechanisms that protect the cells from FasL-induced apoptosis. For the TRAIL receptors, no such downregulation was observed. Here, E5 impairs the formation of the death-inducing signaling complex triggered by TRAIL. Apparently, E5 employs different mechanisms to inhibit death receptor signaling. This effect is not restricted to HaCaT/E5 cells since we found that the mouse fibroblast cell line A31-E5 is protected from TRAIL-induced apoptosis, as well but not the E5-lacking control cells A31-Neo. However, no such protection was observed upon FasL-induced apoptosis. Presumably, some of the antiapoptotic mechanisms employed by E5 of the human pathogenic HPV-16 are cell type specific. We propose that inhibition of ligand-mediated apoptosis in human keratinocytes is a primary function of the HPV-16 E5 protein needed to prevent apoptosis at early stages of viral infection.
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