[No authors listed]
Long nonâcoding 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 miRâ365. The expression of miRâ365 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 miRâ365 abolished the suppressive effect of NEAT1 knockdown on cellular processes. RGS20, a direct target of miRâ365, could reverse the tumor suppressive role of miRâ365 mimic by enhancing cell viability and motility. Moreover, the protein levels of RGS20, cyclin D1, Eâcadherin, Nâcadherin and vimentin could be regulated by the NEAT1/miRâ365 axis. NEAT1 silencing also inhibited tumor growth in vivo. Collectively, we revealed that the NEAT1/miRâ365/RGS20 axis may be a novel mechanism or therapeutic strategy for OSCC treatment.
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