Abstract
Purpose: To examine the potential modulatory mechanisms of NORAD in hepatoma in vitro. 
 Methods: In this study, four human hepatoma cell lines (Bel7404, PLC5, HepG2, and HuH7), as well as a human immortalized Normal MIHA cell line were employed. Transfection was performed to up-or down-regulate NORAD and miR-202-5p expression in cells. RT-qPCR was used to measure expressions of NORAD, miR-202-5p, and biomarkers for cell cycle and apoptosis in HCC cell lines. CCK-8, Flow Cytometry for apoptosis and cell cycle arrest and Western blot experiments were performed to determine cellular viability, cell cycle arrest and apoptosis and related protein expressions. Bioinformatics tool was used to find possible binding sites on NORAD and miR-202-5p, which were further validated by dual-luciferase reporter gene assays. 
 Results: NORAD adversely modulated miR-202-5p in hepatoma cells and mediated cell viability, apoptosis and cell cycle arrest through regulatingmiR-202-5p. Functional experiments revealed that downregulation of NORAD or upregulation of miR-202-5p suppressed cell viability and inhibited apoptosis and cell cycle arrest. Silenced NORAD regulated the EGFR/PI3K/AKT pathway via enhancing miR-202-5p expression in HCC cell lines.
 Conclusion: NORAD interaction with miR-202-5p mediated the EGFR/PI3K/AKT network.
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