Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis
- Jie Wang
- Jingyun Zha
- Xiaolin Wang
Affiliations: Department of Thoracic Surgery, Yangzhou University, Yangzhou, Jiangsu 225000, P.R. China, Department of Respiratory Medicine, Hefei First People's Hospital, Hefei, Anhui 230001, P.R. China
- Published online on: September 20, 2021 https://doi.org/10.3892/ol.2021.13059
Copyright: © Wang
et al. This is an open access article distributed under the
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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.