LncRNA A1BGAS1 Serves as a Tumor Suppressor in Non‐Small Cell Lung Cancer by Modulating the Expression of miR‐3942‐5P

Non-small cell lung cancer (NSCLC), the leading contributor to global cancer mortality, is associated with a notably unfavorable prognosis. This study aims to explore the regulatory interaction between A1BG-AS1 and miR-3942-5p and its molecular mechanisms. The level of A1BG-AS1 and miR-3942-5p in both tumor tissues and cell lines (BEAS-2B, A549, H226) were measured using qPCR. Functional effects of A1BG-AS1 overexpression in NSCLC cells were evaluated through CCK-8, flow cytometry, and Transwell assays. The interaction between A1BG-AS1 and miR-3942-5p was validated through dual-luciferase reporter assays and rescue studies. A1BG-AS1 expression was markedly reduced in both NSCLC tissues and cell lines. A1BG-AS1 expression was significantly associated with various clinical parameters. Overexpression of A1BG-AS1 suppressed NSCLC cell function. Mechanistically, A1BG-AS1 interacted with and negatively regulated miR-3942-5p, and the antitumor effects of A1BG-AS1 overexpression were reversed by miR-3942-5p mimics.A1BG-AS1 inhibits NSCLC tumor progression by targeting miR-3942-5p.

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Publication Details

Journal
Journal of Biochemical and Molecular Toxicology
Published
2026-10-28
DOI
https://doi.org/10.1002/jbt.71151
Primary Topic
Cancer-related molecular mechanisms research
Type
article
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article

LncRNA A1BGAS1 Serves as a Tumor Suppressor in Non‐Small Cell Lung Cancer by Modulating the Expression of miR‐3942‐5P

杜嘉慧, Xuexi Zhang, Chunqiang Wang, Zhenhua Li
Journal of Biochemical and Molecular Toxicology
Cancer-related molecular mechanisms research
article

LncRNA A1BGAS1 Serves as a Tumor Suppressor in Non‐Small Cell Lung Cancer by Modulating the Expression of miR‐3942‐5P

杜嘉慧, Xuexi Zhang, Chunqiang Wang, Zhenhua Li
article en

Abstract

Non-small cell lung cancer (NSCLC), the leading contributor to global cancer mortality, is associated with a notably unfavorable prognosis. This study aims to explore the regulatory interaction between A1BG-AS1 and miR-3942-5p and its molecular mechanisms. The level of A1BG-AS1 and miR-3942-5p in both tumor tissues and cell lines (BEAS-2B, A549, H226) were measured using qPCR. Functional effects of A1BG-AS1 overexpression in NSCLC cells were evaluated through CCK-8, flow cytometry, and Transwell assays. The interaction between A1BG-AS1 and miR-3942-5p was validated through dual-luciferase reporter assays and rescue studies. A1BG-AS1 expression was markedly reduced in both NSCLC tissues and cell lines. A1BG-AS1 expression was significantly associated with various clinical parameters. Overexpression of A1BG-AS1 suppressed NSCLC cell function. Mechanistically, A1BG-AS1 interacted with and negatively regulated miR-3942-5p, and the antitumor effects of A1BG-AS1 overexpression were reversed by miR-3942-5p mimics.A1BG-AS1 inhibits NSCLC tumor progression by targeting miR-3942-5p.

Journal of Biochemical and Molecular ToxicologyVol. 40(11)
Linyi People's Hospital (CN)
Openalex Percentile: Top 16%
Cancer-related molecular mechanisms research
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