Backgrounds: Non-small cell lung cancer (NSCLC) is a highly malignant tumor. Accumulating evidence suggested that long non-coding RNA prostate cancer non-coding RNA 1 (PRNCR1) participated in the pathogenesis of NSCLC, whereas the elaborate mechanism remains not cleared. Hence, the role of PRNCR1 in the progression of NSCLC was investigated. Methods: Levels of PRNCR1, microRNA-126-5p (miR-126-5p), and metadherin (MTDH) were examined by quantitative real-time polymerase chain reaction. Cell

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... feration was measured using Cell Counting Kit-8. Flow cytometry was conducted to determine cell apoptosis. Besides, transwell assay was performed to detect cell migration and invasion in NSCLC cells. The expression levels of E-cadherin, N-cadherin, Vimentin and MTDH were identified via western blot. Dual-luciferase reporter, RNA immunoprecipitation or RNA pull down assays were employed to verify the relationship between miR-126-5p and PRNCR1 or MTDH. Results: PRNCR1 and MTDH levels were high, while miR-126-5p expression was low in NSCLC tissues and cell lines. Knockdown of PRNCR1 promoted cell apoptosis, impeded proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in NSCLC cells, and these effects were abrogated by its target gene of miR-126-5p inhibitor. Moreover, MTDH as the target of PRNCR1, its overexpression reversed the impacts of miR-126-5p mimic on cell behaviors and EMT in vitro. Finally, PRNCR1 and miR-126-5p regulated MTDH expression. Conclusion: PRNCR1 modified cell behaviors and EMT via miR-126-5p/MTDH axis in NSCLC cells, providing a novel thinking for clinical treatment of NSCLC.