ReviewMolecular biology reports2025
Unravelling the molecular crosstalk between Epithelial-Mesenchymal transition and human papillomavirus in oral cancer.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral squamous cell carcinoma (OSCC) is an extremely aggressive malignancy with intricate underlying molecular mechanisms. Emerging evidence suggests that human papillomavirus (HPV) infection, particularly its key oncogenes E6 and E7, can orchestrate epithelial-mesenchymal transition (EMT), a vital process promoting metastasis and tumor growth. HPV oncoproteins can induce EMT by affecting transcription factors like Snail, Twist, and Zeb, and EMT markers (E-cadherin, N-cadherin, and vimentin). These molecular alterations lead to increased invasiveness, stem cell-like properties, and therapeutic resistance in oral cancer, particularly, occurring in the oropharynx. In parallel, epigenetic modifications also play a crucial role in the development and progression of OSCC. Alterations like DNA methylation, histone modifications, chromatin remodelling, and non-coding RNA activity contribute to carcinogenesis by knocking down tumor suppressor genes, disrupting transcriptional regulation, and inducing genomic instability. Aberrant promoter hypermethylation and dysregulated microRNA expression not only facilitate cancer progression but also help in early detection and targeted therapies. This review explores the mechanistic link between HPV-induced EMT and epigenetic regulation in OSCC, highlighting their combined effect on tumor behaviour and therapeutic outcome. Understanding the related molecular pathways in detail could provide new insights into development of novel biomarkers and targeted therapies for HPV-associated oral cancers.
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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.