Comprehensive analysis of gene expression profiles revealed increased expression of genes related to proteasome in feline nasal lymphoma

Feline nasal lymphoma (FNL) is the most common nasal tumor in cats. Although some negative prognostic factors for FNL have been previously reported, further studies on its molecular pathophysiology are needed. In the present study, we conducted comprehensive investigations of gene expression profiles (GEPs) in FNL. GEPs were compared between 17 FNL tissues and peripheral blood mononuclear cell (PBMC) samples of 3 healthy cats by RNA-sequencing. Then, we extracted differentially expressed genes (DEGs), and the differences in their mRNA expression levels were validated by RT-qPCR using 31 FNL, 3 lymph node (LN), and 3 PBMC samples. Finally, immunohistochemistry was performed to validate the expression of the focused protein in 11 FNL tissues and LN of 3 healthy cats. The comparisons of GEPs between FNL and PBMC samples identified 7208 DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that 76 pathways including those related to tumor biology were significantly enriched with DEGs. Part of the extracted pathways commonly included DEGs related to proteasome. RT-qPCR analysis showed a trend toward increased expression of PSMD2 and PSMB5 genes in the FNL samples. In addition, immunohistochemistry also showed that PSMD2 protein expression was comparable and higher when compared with those of germinal centers and other areas of normal lymph nodes, respectively. Our results showed dysregulation of various pathways related to tumor biology and suggested upregulation of genes and proteins related to the proteasome in FNL. Future studies are needed to clarify their associations with the pathogenesis of FNL. • Molecular abnormalities of feline nasal lymphoma (FNL) remain to be clarified. • This study revealed comprehensive gene expression profiles of FNL. • Expressions of genes and protein related to proteasome were upregulated in FNL. • Future studies are needed to examine the roles of proteasome in FNL pathogenesis