Tongue cancer is one of the most common types of cancer, but its molecular etiology and pathogenesis remain unclear. The aim of the present study was to elucidate the pathogenesis of tongue cancer and investigate novel potential diagnostic and therapeutic targets. Four matched pairs of tongue cancer and paracancerous tissues were collected for RNA sequencing (RNA‑Seq), and the differentially expressed genes were analyzed. The RNA‑Seq data of tongue cancer tissues were further analyzed using bioinformatics and reverse transcription‑quantitative PCR analysis. The sequenced reads were quantified and qualified in accordance with the analysis demands. The transcriptomes of the tongue cancer tissues and paired paracancerous tissues were analyzed, and 1,700 upregulated and 2,249 downregulated genes were identified. Gene Ontology analysis uncovered a significant enrichment in the terms associated with extracellular matrix (ECM) organization, cell adhesion and collagen catabolic processes. Kyoto Encyclopedia of Genes and Genomes analysis demonstrated that these differentially expressed genes were mainly enriched in the focal adhesion pathway, ECM‑receptor interaction pathway, phosphoinositide 3‑kinase (PI3K)‑Akt pathway, and cell adhesion molecules. Comprehensive analyses of the gene tree and pathway network revealed that the majority of cell cycle genes were upregulated, while the majority of the genes associated with intracellular response, cell adhesion and cell differentiation were downregulated. The ECM‑receptor interaction, focal adhesion kinase (FAK) and PI3K‑Akt pathways were closely associated with one another and held key positions in differential signaling pathways. The ECM‑receptor, FAK and PI3K‑Akt signaling pathways were found to synergistically promote tongue cancer occurrence and progression, and may serve as potential diagnostic and therapeutic targets for this type of cancer.
Keywords: tongue cancer; RNA sequencing; Gene Ontology analysis; Kyoto Encyclopedia of Genes and Genomes analysis; phosphoinositide 3-kinase-Akt.