ArticleCell & bioscience2024
HPV16 integration regulates ferroptosis resistance via the c-Myc/miR-142-5p/HOXA5/SLC7A11 axis during cervical carcinogenesis.
Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- xCT (Slc7a11) Regulation: Lessons from Cancer Research.Neurochemical research · 2026Pooled it
- Research progress of ferroptosis in cervical cancer treatment.Annals of medicine · 2026Review
- P4HA3 drives cervical cancer lymphatic metastasis by facilitating ACLY-mediated ferroptosis resistance.Cell death and differentiation · 2026Article
- HOXA5 Suppresses NEK7-Mediated Alveolar Epithelial Pyroptosis in Acute Lung Injury by Transcriptionally Inhibiting KAT2A.The Kaohsiung journal of medical sciences · 2026Article
- Article
- Beyond the Limit: MYC Mediates Tumor Immune Escape.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Ferroptosis in human reproductive tract infections and associated disorders: mechanisms and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Exploring the link between serum uric acid and endometriosis: a cross-sectional analysis utilizing NHANES data from 1999-2006.Frontiers in endocrinology · 2025Article
- L-shaped association between dietary iron intake and HPV infection: a cross-sectional analysis based on national health and nutrition examination survey 2005-2016.Frontiers in nutrition · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundFerroptosis, a newly identified form of regulated cell death triggered by small molecules or specific conditions, plays a significant role in virus-associated carcinogenesis. However, whether tumours arising after high-risk HPV integration are associated with ferroptosis is unexplored and remains enigmatic.
methodsHigh-risk HPV16 integration was analysed by high-throughput viral integration detection (HIVID). Ferroptosis was induced by erastin, and the levels of ferroptosis were assessed through the measurement of lipid-reactive oxygen species (ROS), malondialdehyde (MDA), intracellular Fe2
resultsExpression of HPV16 integration hot spot c-Myc negatively correlates with ferroptosis during the progression of cervical squamous cell carcinoma (CSCC). Further investigation revealed that the upregulated oncogene miR-142-5p in HPV16-integrated CSCC cells served as a critical downstream effector of c-Myc in its target network. Inhibiting miR-142-5p significantly decreased the ferroptosis-suppressing effect mediated by c-Myc. Through a combination of computational and experimental approaches, HOXA5 was identified as a key downstream target gene of miR-142-5p. Overexpression of miR-142-5p suppressed HOXA5 expression, leading to decreased accumulation of intracellular Fe2
conclusionsCollectively, these data indicate that HPV16 integration hot spot c-Myc plays a novel and indispensable role in ferroptosis resistance by regulating the miR-142-5p/HOXA5/SLC7A11 signalling axis and suggest a potential therapeutic approach for HPV16 integration-related CSCC.
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