Abstract
Long non‑coding RNAs (lncRNAs) have emerged as critical regulators of tumor progression. However, the function and mechanism of lncRNA NEAT1 in oral squamous cell carcinoma (OSCC) are unclear. In the present study, NEAT1 was significantly upregulated in OSCC cells and tissues. High expression of NEAT1 was correlated with advanced TNM stage and poor survival of patients. Using bioinformatics prediction and experimental analysis, we determined that NEAT1 could negatively regulate the expression of miR‑365. The expression of miR‑365 was decreased in OSCC tissues and inversely correlated with NEAT1 in tumors. Functionally, knockdown of NEAT1 significantly inhibited cell proliferation and invasion and induced cell cycle arrest at the G0/G1 phase and apoptosis, whereas inhibition of miR‑365 abolished the suppressive effect of NEAT1 knockdown on cellular processes. RGS20, a direct target of miR‑365, could reverse the tumor suppressive role of miR‑365 mimic by enhancing cell viability and motility. Moreover, the protein levels of RGS20, cyclin D1, E‑cadherin, N‑cadherin and vimentin could be regulated by the NEAT1/miR‑365 axis. NEAT1 silencing also inhibited tumor growth in vivo. Collectively, we revealed that the NEAT1/miR‑365/RGS20 axis may be a novel mechanism or therapeutic strategy for OSCC treatment.