• Na Huang, Wenjing Dai, Yunhui Li, Jian Sun, Chunlan Ma, and Wancheng Li.
• Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Chengdu Medicine University, Chengdu, Sichuan, China.
• Arch Med Sci. 2020 Jan 1; 16 (5): 1196-1206.

IntroductionLung cancer is the malignant tumor with the fastest increase in morbidity and mortality and the greatest threat to human health and life. Long non-coding RNA (lncRNA) is emerging as an important regulator in many cancers. Recently, it was found that lncRNA prostate cancer associated transcript 1 (PCAT-1) was up-regulated in lung cancer, playing oncogenic roles. However, the underlying regulatory mechanism of PCAT-1 remains unknown.Material And MethodsThe expression levels of PCAT-1 and miR-324-5p were analyzed by real-time PCR, and RAP1A expression was determined by western blotting. RNA pull-down, luciferase and western blotting assays were used to examine the target relationship between PCAT-1 and miR-324-5p or that between miR-324-5p and RAP1A. The functional effects of PCAT-1 and miR-324-5p were examined using cell viability and cell apoptosis assays.ResultsPCAT-1 overexpression remarkably promoted cell proliferation and suppressed cell apoptosis. Mechanistic investigations demonstrated that PCAT-1 can interact with miR-324-5p and repress its expression, thereby increasing the expression of its target RAP1A. Additionally, rescue experiments revealed that PCAT-1 served as an oncogene partly through sponging miR-324-5p and upregulating RAP1A in lung cancer cells.ConclusionsOur findings demonstrate that on account of the dual function of pro-proliferation and anti-apoptosis, PCAT-1/miR-324-5p/RAP1A may be novel candidates for application in the diagnosis, prognosis and therapy of lung cancer.Copyright: © 2019 Termedia & Banach.

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