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Updated: Nov 5, 2025

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
LncRNA PCAT18 Promotes Non-Small Cell Lung Cancer Progression by Sponging miR-4319
Li He1, Jianjun Wang2, Long Zhou3
1Department of Oncology, The People's Hospital of Xinyu City, Xinyu, Jiangxi, People's Republic of China.
Introduction:
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.
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