Human papillomavirus (HPV) is a prevalent sexually transmitted infection, implicated in various cancers, yet its influence in non-cancerous oesophageal tissue remains unclear. This study aims to investigate the gene expression changes associated with high-risk HPV (HR-HPV) in non-cancerous oesophageal tissue to elucidate potential early oncogenic mechanisms. Using RNA sequencing, we compared transcriptomic profiles of HPV-positive and HPV-negative non-cancerous oesophageal tissues. Differential gene expression analysis revealed significant upregulation of cell cycle and DNA replication pathways in HPV-positive samples, specifically involving key genes such as , , and , which are known to regulate cellular proliferation and genomic stability. Additionally, kinase and transcription factor enrichment analyses highlighted HR-HPV-associated regulatory molecules, including E2F4 and CSNK2A1, suggesting HPV's role in modulating host cell cycle control. These findings support the hypothesis that HPV infection may initiate cellular alterations in oesophageal tissue, potentially predisposing it to malignancy. This study contributes to understanding HPV's impact in non-cancerous tissues and identifies possible biomarkers for early HPV-related cellular changes, offering insights into HPV-driven cancer development beyond traditionally associated sites.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11720088PMC
http://dx.doi.org/10.3390/ijms26010056DOI Listing

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