ArticleCell death and differentiation2024
Activating STING/TBK1 suppresses tumor growth via degrading HPV16/18 E7 oncoproteins in cervical cancer.
Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- HPV16 E7 Enhances Cell Stemness via RTKN2-Mediated Activation of the NF-κB Pathway in Cervical Cancer.Biochemical genetics · 2026Article
- Reprogramming the tumor immune microenvironment in cervical cancer: synergy between radiotherapy and immunotherapy.Molecular cancer · 2026Review
- Antitumor effects of STING agonists on nervous system tumors via tumor-intrinsic STING-STAT1-mediated HMGN2 expression.Cancer biology & medicine · 2026Article
- Ubiquitin-centered post-translational modification crosstalk orchestrates tumor immunity and immunotherapy response.Experimental hematology & oncology · 2026Review
- Different Expressions and Methylation Patterns of cGAS and STING in Cervical Cancer.Obstetrics and gynecology international · 2026Article
- Mitochondrial reprogramming in cervical cancer: crosstalk with tumor immunity, HPV oncogenic signaling, and therapeutic resistance.Frontiers in immunology · 2026Review
- Spatially organized macrophage-T-cell crosstalk in cervical cancer: insights from single-cell and spatial omics.Frontiers in immunology · 2026Review
- KDM5B recruits FOXG1 to suppress the IFN response, leading to malignant progression and immune evasion in cervical cancer.Frontiers in medicine · 2026Article
- Innate immune recognition and microenvironmental reprogramming in HPV-induced cervical cancer: from pattern recognition receptor activation to immune tolerance disruption.Frontiers in cellular and infection microbiology · 2026Review
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- PRRSV evades innate immune cGAS-STING antiviral function via its Nsp5 to deter STING translocation and activation.Virulence · 2025Article
- Protein-S-nitrosylation of adenovirus-5 E1A and human papillomavirus 16 E7 limits their ability to inhibit STING activity.Journal of virology · 2025Article
- The immune microenvironment of pathogen-associated cancers and current clinical therapeutics.Molecular cancer · 2025Review
- BAG2 Inhibits Cervical Cancer Progression by Modulating Type I Interferon Signaling through Stabilizing STING.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of innate immunity triggered by HPV infection in promoting cervical lesions.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Molecular Insights into HPV-Driven Cervical Cancer: Oncoproteins, Immune Evasion, and Epigenetic Modifications.Microorganisms · 2025Review
- Review
- cGAS/STING signaling pathway in gynecological malignancies: From molecular mechanisms to therapeutic values.Frontiers in immunology · 2025Review
- Canagliflozin as a Potential Preclinical Therapy for Tuberous Sclerosis Complex: Inhibition ofDrug design, development and therapy · 2025Article
- The role of cGAS-STING signaling in HPV infection and HPV-related cancers.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Cervical cancer is the most common gynecologic cancer, etiologically related to persistent infection of human papillomavirus (HPV). Both the host innate immunity system and the invading HPV have developed sophisticated and effective mechanisms to counteract each other. As a central innate immune sensing signaling adaptor, stimulator of interferon genes (STING) plays a pivotal role in antiviral and antitumor immunity, while viral oncoproteins E7, especially from HPV16/18, are responsible for cell proliferation in cervical cancer, and can inhibit the activity of STING as reported. In this report, we find that activation of STING-TBK1 (TANK-binding kinase 1) promotes the ubiquitin-proteasome degradation of E7 oncoproteins to suppress cervical cancer growth. Mechanistically, TBK1 is able to phosphorylate HPV16/18 E7 oncoproteins at Ser71/Ser78, promoting the ubiquitination and degradation of E7 oncoproteins by E3 ligase HUWE1. Functionally, activated STING inhibits cervical cancer cell proliferation via down-regulating E7 oncoproteins in a TBK1-dependent manner and potentially synergizes with radiation to achieve better effects for antitumor. Furthermore, either genetically or pharmacologically activation of STING-TBK1 suppresses cervical cancer growth in mice, which is independent on its innate immune defense. In conclusion, our findings represent a new layer of the host innate immune defense against oncovirus and provide that activating STING/TBK1 could be a promising strategy to treat patients with HPV-positive cervical cancer.
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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.