The lncRNA NORAD/miR-520a-3p Facilitates Malignancy in Non-Small Cell Lung Cancer via PI3k/Akt/mTOR Signaling Pathway

OncoTargets and Therapy. 2020;Volume 13:1533-1544

 

Journal Homepage

Journal Title: OncoTargets and Therapy

ISSN: 1178-6930 (Online)

Publisher: Dove Medical Press

LCC Subject Category: Medicine: Internal medicine: Neoplasms. Tumors. Oncology. Including cancer and carcinogens

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS


Wan Y

Yao Z

Chen W

Li D

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 16 weeks

 

Abstract | Full Text

Yunyan Wan, Zhouhong Yao, Weijuan Chen, Dezhi Li Department of Respiratory and Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, People’s Republic of ChinaCorrespondence: Dezhi LiDepartment of Respiratory and Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong University, No. 324 Jingwuweiqi Road, Jinan, Shandong 250021, People’s Republic of ChinaEmail [email protected]/Aims: The effects of lncRNA-NORAD/mir-520a-3p on proliferation and invasion of non-small cell lung cancer (NSCLC) were studied, and its potential molecular mechanism was discussed.Methods: qRT-PCR was used to detect the expression of lncRNA NORAD and miR-520a-3p in non-small cell lung cancer tissues and cell lines. CCK-8 method and Transwell test were used to identify the effects of lncRNA NORAD on the proliferation and invasion in NSCLC. Target gene prediction and screening and luciferase reporter assay was used to verify downstream target genes of lncRNA NORAD. The expressions of PI3K, AKT, and mTOR proteins were detected by Western blot.Results: Compared with normal tissues and cells, the expressions of lncRNA NORAD in cancer tissues and cells were significantly higher. Compared with normal cells, the expression of miR-520a-3p in cells was considerably lower. LncRNA NORAD could accelerate the growth and metastasis of NSCLC in vitro and in vivo. Luciferase reporter assay results indicated that miR-520a-3p was a downstream target gene of lncRNA NORAD. Further findings showed that lncRNA NORAD might bind to miR-520a-3p, thereby affecting the PI3k/Akt/mTOR signaling pathway.Conclusion: LncRNA NORAD can regulate the proliferation of NSCLC by regulating miR-520a-3p/PI3k/Akt/mTOR signaling pathway, thus promoting the occurrence and development of NSCLC.Keywords: non-small cell lung cancer, lncRNA NORAD, miR-520a-3p, PI3k/Akt/mTOR, proliferation