ArticleCell cycle (Georgetown, Tex.)2013
Liberation of functional p53 by proteasome inhibition in human papilloma virus-positive head and neck squamous cell carcinoma cells promotes apoptosis and cell cycle arrest.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Noncanonical Pathways of Proteasome Inhibition in HPV-Negative Head & Neck Cancer.Molecular carcinogenesis · 2025Article
- Daidzein enhances cisplatin sensitivity and inhibits migration of oral squamous cell carcinoma through modulating mitogen-activated protein kinase signaling pathway.Journal of dental sciences · 2025Article
- Developments and future prospects of personalized medicine in head and neck squamous cell carcinoma diagnoses and treatments.Cancer reports (Hoboken, N.J.) · 2024Review
- Small Molecule Inhibitors of Human Papillomavirus: A Review of Research from 1997 to 2021.Current medicinal chemistry · 2024Review
- Article
- Review
- Hyperactivating p53 in Human Papillomavirus-Driven Cancers: A Potential Therapeutic Intervention.Molecular diagnosis & therapy · 2022Review
- Proteasome inhibition by bortezomib parallels a reduction in head and neck cancer cells growth, and an increase in tumor-infiltrating immune cells.Scientific reports · 2021Article
- NF-Y Subunits Overexpression in HNSCC.Cancers · 2021Article
- Ethanol Extracts ofJournal of immunology research · 2021Article
- p53 Is Regulated in a Biphasic Manner in Hypoxic Human Papillomavirus Type 16 (HPV16)-Positive Cervical Cancer Cells.International journal of molecular sciences · 2020Article
- Current Prospects of Molecular Therapeutics in Head and Neck Squamous Cell Carcinoma.Pharmaceutical medicine · 2019Review
- In HPV-Positive HNSCC Cells, Functional Restoration of the p53/p21 Pathway by Proteasome Inhibitor Bortezomib Does Not Affect Radio- or Chemosensitivity.Translational oncology · 2019Article
- Positioning of proteasome inhibitors in therapy of solid malignancies.Cancer chemotherapy and pharmacology · 2018Review
- Curcumin-Mediated Degradation of S-Phase Kinase Protein 2 Induces Cytotoxic Effects in Human Papillomavirus-Positive and Negative Squamous Carcinoma Cells.Frontiers in oncology · 2018Article
- TRIP12 as a mediator of human papillomavirus/p16-related radiation enhancement effects.Oncogene · 2017Article
- A Small Molecule Inhibitor Selectively Induces Apoptosis in Cells Transformed by High Risk Human Papilloma Viruses.PloS one · 2016Article
- Increased sensitivity of HPV-positive head and neck cancer cell lines to x-irradiation ± Cisplatin due to decreased expression of E6 and E7 oncoproteins and enhanced apoptosis.American journal of cancer research · 2015Article
- Wild-type p53 reactivation by small-molecule Minnelide™ in human papillomavirus (HPV)-positive head and neck squamous cell carcinoma.Oral oncology · 2014Article
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2 authors at 2 institutions in 1 country.
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Abstract
Human papilloma virus (HPV) infection represents an emerging risk factor in head and neck squamous cell carcinoma (HNSCC). In contrast to HPV-negative HNSCC, most cases of HPV-positive HNSCC encode wild-type p53, although the p53 protein in these cells is rapidly degraded via HPV E6-mediated ubiquitination and subsequent proteasomal degradation. This unique feature of HPV-positive HNSCC has raised hope that liberation of wild-type p53 from the E6 protein may have therapeutic benefit in this disease. Indeed, suppression of E6 expression promotes apoptosis in HPV-positive HNSCC cell lines. However, the role of p53 in mediating this cell death has not been determined. Here, we demonstrate that siRNAs targeting the E6/E7 RNA, or treatment with the proteasome inhibitor bortezomib, resulted in upregulation of functional p53 and p53 gene targets in three HPV-positive HNSCC cell lines, but not in HPV-negative HNSCC cells. Apoptosis induced by E6/E7 siRNA in HPV-positive cells was found to be dependent on p53, while bortezomib-induced cell death was modestly p53-dependent. Treatment with subtoxic doses of bortezomib led to cell cycle arrest in HPV-positive, but not HPV-negative HNSCC cells. Moreover, this cell cycle arrest was mediated by p53 and the cell cycle inhibitor p21, the product of a p53 target gene. Collectively, these findings establish that wild-type p53 encoded by HPV-positive HNSCC cells, once liberated from HPV E6, can play important roles in promoting apoptosis and cell cycle arrest.
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