Unravelling the role of EMT in OSCC: A quick peek into HPV-mediated pathogenesis

Abstract

Oral squamous cell carcinoma (OSCC) is a highly invasive and pervasive human oral neoplasia, accounting for approximately 90% of all oral cavity carcinomas worldwide. Despite technological advancements, tumor spread and consequent relapse result in meagre 5- year survival rates of less than 60%. Metastasis is the culmination of a multiphase transition, characterized as epithelial-to-mesenchymal transition (EMT), which stipulates gradual acquisition of migratory phenotype in epithelial cells. Physiologically, EMT is a transient and a dynamic phenomenon underlying wound healing. However, chronic exposure of oral epithelium to multiple irritants and pathogens such as high risk-human papillomavirus (HR-HPV), causes EMT to be predominantly stimulated leading to metastatic and/or recurrent OSCC. The dreadful clinical manifestations, together with our growing understanding of EMT in carcinogenesis has prompted us to conduct a comprehensive literature review on EMT in OSCC, addressing issues such as the disruption of intercellular junctions and cytoskeleton, idiosyncratic behavior of cellular markers and signaling pathways, and tumoral microvascular environment involving inflammatory cytokines, with an insight into the role of HPV infection as a model risk factor in OSCC.

Keywords

• Oral squamous cell carcinoma (OSCC)
• Epithelial-to-mesenchymal transition (EMT)
• Biomarkers
• Tumor microenvironment
• Human papilloma virus (HPV)