Cancer Management and Research (May 2021)

LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319

  • He L,
  • Wang J,
  • Zhou L,
  • Li X

Journal volume & issue
Vol. Volume 13
pp. 3761 – 3774

Abstract

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Li He,1 Jianjun Wang,2 Long Zhou,3 Xiaobing Li1 1Department of Oncology, The People’s Hospital of Xinyu City, Xinyu, Jiangxi, People’s Republic of China; 2Department of Radiology, Haiyan People’s Hospital, Jiaxing, Zhejiang, People’s Republic of China; 3Department of Radiation Oncology, Xiangtan Central Hospital, Xiangtan, Hunan, People’s Republic of ChinaCorrespondence: Xiaobing LiDepartment of Oncology, The People’s Hospital of Xinyu City, 369 Xinxinbei Road, Xinyu, Jiangxi, 330008, People’s Republic of ChinaEmail [email protected]: NSCLC (non-small cell lung cancer), the most common type of human cancer, is a main cause of cancer-associated mortality. Accumulating evidence has confirmed that long non-coding RNAs serve crucial roles in NSCLC development.Methods: The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319.Results: PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo.Conclusion: In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC.Keywords: PCAT18, miR-4319, non-small cell lung cancer, invasion, proliferation

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