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Original Research Article | OPEN ACCESS

LncRNA NORAD/miR-202-5p regulates hepatoma cell viability, apoptosis via EGFR/PI3K/AKT signaling pathway

Xiaoling Wei1 , Lingjun Dong2, Xiubing Lei3

1Department of Oncology, Pengshan District People's Hospital, Meishan City. Sichuan 620860, China; 2Department of Orthopedics, Pengshan District People's Hospital, Meishan City. Sichuan 620860, China; 3School of Basic Medicine, Panzhihua University, Sichuan 617000, China.

For correspondence:-  Xiaoling Wei   Email: fd85457@126.com

Accepted: 30 March 2023        Published: 29 April 2023

Citation: Wei X, Dong L, Lei X. LncRNA NORAD/miR-202-5p regulates hepatoma cell viability, apoptosis via EGFR/PI3K/AKT signaling pathway. Trop J Pharm Res 2023; 22(4):749-757 doi: 10.4314/tjpr.v22i4.6

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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 regulating miR-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.

Keywords: Apoptosis, Cell viability, EGFR/PI3K/AKT signaling, MiR-202-5p, NORAD

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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