Feline Nasal Planum Squamous Cell Carcinoma: interaction between Feline Papillomavirus infection and Epithelial–Mesenchymal Transition

Feline nasal planum squamous cell carcinoma (npSCC) is a locally aggressive neoplasm of great relevance in veterinary oncology. Beyond its clinical relevance in cats, npSCC has attracted growing interest as a potential comparative model for human papillomavirus (HPV)-associated carcinomas, for its histopathological and molecular similarities. In particular, the detection of viral DNA and transcriptional activity of viral oncogenes in feline SCC suggests a biologically active role rather than incidental infection. At the same time, epithelial-mesenchymal transition (EMT) has been recognized as an important process in the progression and invasiveness of squamous cell carcinomas across species. However, the interplay between FcaPV infection and EMT activation in feline npSCC remains incompletely defined, representing an important topic of study with both clinical and comparative oncology implications. The aim of the study was to investigate the prevalence and transcriptional activity of FcaPV in feline npSCC, the expression of EMT markers and to explore associations between viral infection status and EMT features. Fifty feline npSCC and ten control tissues were examined by PCR and RT-PCR for FcaPV DNA and E6/E7 transcription, and by immunohistochemistry for epithelial, mesenchymal, EMT transcription factors and hypoxia/-catenin pathway markers. FcaPV DNA was detected in 64% of npSCC, predominantly FcaPV-2. Viral transcription was confirmed in 95% of L1-positive tumors, supporting biologically active infection. Immunohistochemistry revealed EMT features, including loss of epithelial markers, vimentin acquisition and focal nuclear expression of TWIST-1 and ZEB1. However, no significant differences in EMT markers expression were found between FcaPV-positive and FcaPV-negative tumors. These findings confirm that FcaPV is actively involved in feline npSCC, but EMT activation appears as a common feature of SCC progression independent of viral status. Further studies are needed to continue to evaluate feline npSCC as a model for studying PV-induced tumorigenesis in perspective.