ArticleOncology letters2021
Knockdown of lncRNA NUTM2A-AS1 inhibits lung adenocarcinoma cell viability by regulating the miR-590-5p/METTL3 axis.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- TFAP2A-Induced Upregulation of LncRNA NUTM2A-AS1 Promotes LUAD Progression Through a miR-409-5p/SLC35F2 Regulatory Axis.Journal of cellular and molecular medicine · 2026Article
- NUTM2A-AS1 as a potential key regulator in cancer: unraveling its ceRNA networks and impact on tumor biology.European journal of medical research · 2025Review
- A novel NUTM2A-AS1/miR-769-5p axis regulates LPS-evoked damage in human dental pulp cells via the TLR4/MYD88/NF-κB signaling.Journal of dental sciences · 2025Article
- Accurate fusion transcript identification from long- and short-read isoform sequencing at bulk or single-cell resolution.Genome research · 2025Article
- Association between methyltransferase-like 3 and non-small cell lung cancer: pathogenesis, therapeutic resistance, and clinical applications.Translational lung cancer research · 2024Review
- LncRNA NUTM2A-AS1 silencing inhibits glioma via miR-376a-3p/YAP1 axis.Cell division · 2024Article
- CTAT-LR-fusion: accurate fusion transcript identification from long and short read isoform sequencing at bulk or single cell resolution.bioRxiv : the preprint server for biology · 2024Article
- H3K27ac-activated LncRNA NUTM2A-AS1 Facilitated the Progression of Colorectal Cancer CellsCurrent cancer drug targets · 2024Article
- Using integrated analysis from multicentre studies to identify RNA methylation-related lncRNA risk stratification systems for glioma.Cancer cell international · 2023Article
- Review
- Novel insights into mutual regulation between NCancer cell international · 2023Review
- circ_0020123 promotes cell proliferation and migration in lung adenocarcinoma via PDZD8.Open medicine (Warsaw, Poland) · 2022Article
- An m6A/m5C/m1A/m7G-Related Long Non-coding RNA Signature to Predict Prognosis and Immune Features of Glioma.Frontiers in genetics · 2022Article
Corrections and comments
- Retraction · 2025-12-08Author Unresponsive · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Data · Plagiarism of Image · · See also: https://pubpeer.com/publications/017101372D2FDC2D75908142F6DA10
- Retracted
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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