ArticleCancers2020
Human Papillomavirus 16 E7 Promotes EGFR/PI3K/AKT1/NRF2 Signaling Pathway Contributing to PIR/NF-κB Activation in Oral Cancer Cells.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Molecular, immunological and oncogenic mechanisms of cervical cancer mediated by HPV/HIV co-infection, clinical implication and management.Infectious agents and cancer · 2025Review
- Structural and Functional Insights into Viral and Fungal Proteins Involved in Chronic Inflammation and Their Biologic Treatments.Pharmaceutics · 2025Review
- Attributes of HPV associated cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.Molecular pharmacology · 2025Article
- Current challenges and potential opportunities for interception and prevention of head and neck cancer.Carcinogenesis · 2025Review
- Roles of human papillomavirus in cancers: oncogenic mechanisms and clinical use.Signal transduction and targeted therapy · 2025Review
- Article
- Article
- Ferroptosis-immune crosstalk in cervical cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- SLC7A11 Expression Is Up-Regulated in HPV- and Tobacco-Associated Lung Cancer.International journal of molecular sciences · 2024Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.bioRxiv : the preprint server for biology · 2024Article
- Identification of proteins' expression pathway and the effective miRNAs for the treatment of human papillomavirus-induced cervical cancer: in-silico analyses-experimental research.Annals of medicine and surgery (2012) · 2024Article
- Epstein-Barr Virus BARF1 Is Expressed in Lung Cancer and Is Associated with Cancer Progression.Cells · 2024Article
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- Protective Effect and Related Mechanism of Modified Danggui Buxue Decoction on Retinal Oxidative Damage in Mice based on Network Pharmacology.Current pharmaceutical design · 2024Article
- Mechanisms of action of Fu Fang Gang Liu liquid in treating condyloma acuminatum by network pharmacology and experimental validation.BMC complementary medicine and therapies · 2023Article
- Interaction between Cigarette Smoke and Human Papillomavirus 16 E6/E7 Oncoproteins to Induce SOD2 Expression and DNA Damage in Head and Neck Cancer.International journal of molecular sciences · 2023Article
- Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways.PloS one · 2023Article
- Characterization of High-Risk HPV/EBV Co-Presence in Pre-Malignant Cervical Lesions and Squamous Cell Carcinomas.Microorganisms · 2022Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
A subset of oral carcinomas is etiologically related to high-risk human papillomavirus (HR-HPV) infection, with HPV16 being the most frequent HR-HPV type found in these carcinomas. The oncogenic role of HR-HPV is strongly dependent on the overexpression of E6 and E7 oncoproteins, which, in turn, induce p53 and pRb degradation, respectively. Additionally, it has been suggested that HR-HPV oncoproteins are involved in the regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), inducing cancer progression and metastasis. Previously, we reported that HPV16 E7 oncoprotein promotes Pirin upregulation resulting in increased epithelial-mesenchymal transition (EMT) and cell migration, with Pirin being an oxidative stress sensor and activator of NF-κB. In this study, we demonstrate the mechanism by which HPV16 E7-mediated Pirin overexpression occurs by promoting EGFR/PI3K/AKT1/NRF2 signaling, thus causing PIR/NF-κB activation in oral tumor cells. Our results demonstrate a new mechanism by which E7 contributes to oral cancer progression, proposing PIR as a potential new therapeutic target.
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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.