ArticleCarcinogenesis2015
HPV16 E6 and E7 proteins induce a chronic oxidative stress response via NOX2 that causes genomic instability and increased susceptibility to DNA damage in head and neck cancer cells.
Article in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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Who cites it
59 citing papers in PubMed, 95 citations in OpenAlex.
- Viral Comorbidities Remodel Host Transcriptome and Redox Signaling in an NADPH Oxidase Isoform-Specific Manner.Viruses · 2026Review
- HPV Infection and Oxidative Stress in Cervical Carcinogenesis: Linking Apoptosis, Senescence, SASP, and EMT.Antioxidants (Basel, Switzerland) · 2026Review
- Up-regulation of peroxiredoxin 3 by high-risk human papillomavirus in cervical cancer cells.Archives of medical science : AMS · 2026Article
- Inflammasomes meet organoids and artificial intelligence: unraveling the complexity of gynecological inflammation.Frontiers in immunology · 2026Review
- Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation.Redox report : communications in free radical research · 2025Article
- From Carcinogenesis to Drug Resistance: The Multifaceted Role of Oxidative Stress in Head and Neck Cancer.Cancers · 2025Review
- From infection to infertility: a review of the role of human papillomavirus-induced oxidative stress on reproductive health and infertility.European journal of medical research · 2025Review
- Oxidative Stress and Dietary Antioxidants in Head and Neck Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- Development and validation of a multiplex qPCR method for identification of high-risk genotypes of human papillomavirus.Infectious agents and cancer · 2025Article
- Patterns of immune cell infiltration and oxidative stress in cervical cancer.Oncology reviews · 2025Review
- Emerging paradigms: unmasking the role of oxidative stress in HPV-induced carcinogenesis.Infectious agents and cancer · 2024Review
- The Causes and Consequences of DNA Damage and Chromosomal Instability Induced by Human Papillomavirus.Cancers · 2024Review
- Dysregulation of base excision repair factors associated with low tumor immunogenicity in head and neck cancer: implication for immunotherapy.Therapeutic advances in medical oncology · 2024Article
- Altered mitochondrial DNA copy number in cervical exfoliated cells among high‑risk HPV‑positive and HPV‑negative women.Experimental and therapeutic medicine · 2023Article
- Contributions of viral oncogenes of HPV-18 and hypoxia to oxidative stress and genetic damage in human keratinocytes.Scientific reports · 2023Article
- Human papillomavirus E6/E7 oncoproteins promote radiotherapy-mediated tumor suppression by globally hijacking host DNA damage repair.Theranostics · 2023Article
- Dietary artemisinin boosts intestinal immunity and healthy in fat greenling (Frontiers in immunology · 2023Article
- Beta Human Papillomavirus 8 E6 Induces Micronucleus Formation and Promotes Chromothripsis.Journal of virology · 2022Article
- The Drivers, Mechanisms, and Consequences of Genome Instability in HPV-Driven Cancers.Cancers · 2022Review
- The World of Oral Cancer and Its Risk Factors Viewed from the Aspect of MicroRNA Expression Patterns.Genes · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Human papillomavirus (HPV) is the causative agent of a subgroup of head and neck cancer characterized by an intrinsic radiosensitivity. HPV initiates cellular transformation through the activity of E6 and E7 proteins. E6 and E7 expression is necessary but not sufficient to transform the host cell, as genomic instability is required to acquire the malignant phenotype in HPV-initiated cells. This study reveals a key role played by oxidative stress in promoting genomic instability and radiosensitivity in HPV-positive head and neck cancer. By employing an isogenic human cell model, we observed that expression of E6 and E7 is sufficient to induce reactive oxygen species (ROS) generation in head and neck cancer cells. E6/E7-induced oxidative stress is mediated by nicotinamide adenine dinucleotide phosphate oxidases (NOXs) and causes DNA damage and chromosomal aberrations. This mechanism for genomic instability distinguishes HPV-positive from HPV-negative tumors, as we observed NOX-induced oxidative stress in HPV-positive but not HPV-negative head and neck cancer cells. We identified NOX2 as the source of HPV-induced oxidative stress as NOX2 silencing significantly reduced ROS generation, DNA damage and chromosomal aberrations in HPV-positive cells. Due to their state of chronic oxidative stress, HPV-positive cells are more susceptible to DNA damage induced by ROS and ionizing radiation (IR). Furthermore, exposure to IR results in the formation of complex lesions in HPV-positive cells as indicated by the higher amount of chromosomal breakage observed in this group of cells. These results reveal a novel mechanism for sustaining genomic instability in HPV-positive head and neck tumors and elucidate its contribution to their intrinsic radiosensitivity.
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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.