Sinonasal squamous cell carcinoma (SNSCC) is one of the least frequent carcinomas in the head and neck and accounts for 60% to 75% of sinonasal malignancies. The role of long non-coding RNAs (lncRNAs) in cancer development has drawn great attention over the years. The current study intended to assess the role and specific mechanism of lncRNA double homeobox A pseudogene 8 (DUXAP8) in SNSCC. Quantitative real-time PCR (qRT-PCR) analysis was implemented to assess the expression level of DUXAP8, microRNA-584-5p (miR-584-5p), and fibronectin type III domain containing 3B (FNDC3B). Proliferation assays included colony formation assay, Cell Counting Kit-8 (CCK-8) assay, and 5-ethynyl-2'-deoxyuridine (EdU) assay. Transwell assays were implemented to monitor cell migration and invasion. Cell apoptosis was evaluated via terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and JC-1 experiments. Mechanism experiments included RNA pull-down assay, RNA binding protein immunoprecipitation (RIP) assay, and luciferase reporter assay. DUXAP8 is overexpressed in SNSCC cells. Functionally, DUXAP8 silencing suppresses the malignant progression of SNSCC. Furthermore, DUXAP8 up-regulates the expression of FNDC3B via sponging miR-584-5p. Rescue experiments demonstrated that DUXAP8 mediates the progression of SNSCC via up-regulating FNDC3B expression. In conclusion, DUXAP8 acts as an oncogene in SNSCC, which may be a new molecular marker for SNSCC.
Keywords: DUXAP8; FNDC3B; miR-584-5p; sinonasal squamous cell carcinoma.