Long Non-Coding RNA NEAT1 Accelerates Lung Cancer Development Via MicroRNA-107/FOXK1 Axis

Abstract Objective: Studies have abstracted the partial mechanism of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) in lung cancer, but its reciprocal with microRNA-107/Forkhead box k1 (miR-107/FOXK1) is not disclosed clearly. Hence, the mechanism of NEAT1/miR-107/FOXK1 was delved out in lung cancer.Methods: NEAT1, miR-107 and FOXK1 expression in clinical cancer tissues were determined, along with their interactions. The relation between the survival of lung cancer patients and NEAT1 expression was determined. NEAT1 and/or miR-107-related lentivirus or plasmid were transfected into A549 cells, after which cell biological functions were tested. Tumors were xenografted in mice to observe tumor formation and cell apoptosis.Results: High NEAT1 and FOXK1 and low miR-107 levels were tested in lung cancer tissues. High NEAT1 was connected with low overall survival of lung cancer patients. Depleting NEAT1 or augmenting miR-107 inhibited the biological functions of lung cancer cells. Depleted NEAT1 suppressed tumor-forming ability of A549 cells in vivo. Inhibited miR-107 antagonized depleted NEAT1-mediated effects on A549 cells. NEAT1 regulated FOXK1 by competitively binding miR-107.Conclusion: Silenced NEAT1 suppresses lung cancer development through elevating miR-107 and reducing FOXK1 expression, which supplies a plan to treat lung cancer.