ArticleMolecular genetics & genomic medicine2020
MiR-338 regulates NFATc1 expression and inhibits the proliferation and epithelial-mesenchymal transition of human non-small-cell lung cancer cells.
Article in Molecular genetics & genomic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Spatial transcriptomics defines IM-crypt as a premalignant niche with bidirectional divergence in early gastric carcinogenesis.Communications biology · 2026Article
- NFATc1 activates the Ras/Raf/p38 MAPK pathway to promote the progression of lung adenocarcinoma.Translational cancer research · 2025Article
- Proliferation, apoptosis and invasion of human lung cancer cells are associated with NFATc1.Experimental and therapeutic medicine · 2023Article
- Epigenetic mechanisms of lung carcinogenesis involve differentially methylated CpG sites beyond those associated with smoking.European journal of epidemiology · 2022Article
- Article
- Molecular interactions of miR-338 during tumor progression and metastasis.Cellular & molecular biology letters · 2021Review
- MiR-338 regulates NFATc1 expression and inhibits the proliferation and epithelial-mesenchymal transition of human non-small-cell lung cancer cells.Molecular genetics & genomic medicine · 2020Article
- circRAE1 promotes colorectal cancer cell migration and invasion by modulating miR-338-3p/TYRO3 axis.Cancer cell international · 2020Article
- MicroRNA-374b-5p Functions as a Tumor Suppressor in Non-Small Cell Lung Cancer by Targeting FOXP1 and Predicts Prognosis of Cancer Patients.OncoTargets and therapy · 2020Article
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Authors and funding
2 authors.
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Abstract
backgroundIt is well known that nuclear factor of activated T cells c1 (NFATc1) expression is closely associated with progression of many cancers. And we found that miR-338 could directly target the NFATc1. However, the precise mechanisms of miR-338 in non-small-cell lung cancer (NSCLC) have not been well clarified. Our study aimed to explore the interaction between NFATc1 and miR-338 in NSCLC.
methodsQuantitative RT-PCR was utilized to determine the expressions of NFATc1 and miR-338 in NSCLC tissues and cell lines. And the cell proliferation and epithelial-mesenchymal transition (EMT) were assessed to determine the functional roles of miR-338 and NFATc1 in NSCLC cells. NFATc1 expression was detected using quantitative RT-PCR and western blotting, respectively. Luciferase reporter assays were performed to validate NFATc1 as a target of miR-338 in NSCLC cells.
resultsIn this study, our results showed that NFATc1 expression was significantly up-regulated in NSCLC tissues and cell lines, and the miR-338 level was dramatically down-regulated. Moreover high NFATc1 expression was closely associated with low miR-338 level in NSCLC tissues. Moreover introduction of miR-338 significantly inhibited proliferation and EMT of NSCLC cells. Bioinformatics analysis predicted that the NFATc1 was a potential target gene of miR-338. We demonstrated that miR-338 could directly target NFATc1 by using luciferase reporter assay. Besides, knockdown of NFATc1 had the similar effects with miR-338 overexpression on NSCLC cells. Up-regulation of NFATc1 in NSCLC cells partially abolished the inhibitory effects of miR-338 mimic.
conclusionsOverexpression of miR-338 inhibited cell proliferation and EMT of NSCLC cells by directly down-regulating NFATc1 expression.
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