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Knockdown of lncRNA NUTM2A-AS1 inhibits lung adenocarcinoma cell viability by regulating the miR-590-5p/METTL3 axis

Authors
  • Wang, Jie1
  • Zha, Jingyun2
  • Wang, Xiaolin1
  • 1 Department of Thoracic Surgery, Yangzhou University, Yangzhou, Jiangsu 225000, P.R. China
  • 2 Department of Respiratory Medicine, Hefei First People's Hospital, Hefei, Anhui 230001, P.R. China
Type
Published Article
Journal
Oncology Letters
Publisher
Spandidos Publications
Publication Date
Sep 20, 2021
Volume
22
Issue
5
Identifiers
DOI: 10.3892/ol.2021.13059
PMID: 34630705
PMCID: PMC8477074
Source
PubMed Central
Keywords
Disciplines
  • Articles
License
Unknown

Abstract

Lung adenocarcinoma (LUAD) is the leading cause of cancer-related mortality worldwide. Long non-coding RNA (lncRNA) NUT family member 2A antisense RNA 1 (NUTM2A-AS1) is dysregulated in LUAD; however, its role in this disease remains unclear. The present study aimed to identify the underlying molecular mechanism of the effect of lncRNA NUTM2A-AS1 in LUAD by exploring whether lncRNA NUTM2A-AS1 could affect LUAD cell proliferation and apoptosis through the microRNA (miR)-590-5p/methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit (METTL3) axis. miR-590-5p was predicted and verified as the direct target of NUTM2A-AS1 using bioinformatics analysis and a dual luciferase reporter assay. The expression levels of NUTM2A-AS1 and miR-590-5p in lung cancer cells, and the effects of NUTM2A-AS1 on cell viability and apoptosis were determined using MTT assays and flow cytometry, respectively. Reverse transcription-quantitative PCR analysis revealed that the expression levels of NUTM2A-AS1 were significantly upregulated, while those of miR-590-5p were significantly downregulated, in lung cancer cells compared with the control epithelial cells. NUTM2A-AS1 knockdown inhibited NCI-H23 cell viability and induced apoptosis by upregulating miR-590-5p expression. Moreover, the function and regulatory mechanism of miR-590-5p in LUAD were also investigated. It was determined that miR-590-5p could interact with METTL3, and further analysis of the expression levels of METTL3 in lung cancer cells demonstrated that METTL3 was significantly upregulated in NCI-H23 and A549 cells compared with the control cells. In addition, miR-590-5p inhibited NCI-H23 cell viability and induced apoptosis by downregulating METTL3 expression. In conclusion, the findings of the present study suggested that NUTM2A-AS1 knockdown may inhibit LUAD progression by regulating the miR-590-5p/METTL3 axis. These results may provide insight into the mechanisms underlying the tumorigenesis of LUAD and offer a new treatment strategy for the disease.

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