ArticleHuman molecular genetics2023
Tumor suppressor genes are reactivated by miR-26A1 via enhancer reprogramming in NSCLC.
Article in Human molecular genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- The paradox of nuclear miRNAs: Mechanisms, therapeutic potential, and future directions.Non-coding RNA research · 2026Review
- Current Insights and Future Directions of Multiomic and Spatial-Omic Analysis in Non-Small Cell Lung Cancer.JCO precision oncology · 2026Review
- The Multi-Target lncRNA-miRNA-mRNA TRIAD in Pancreatic Cancer Diagnosis and Therapy.International journal of molecular sciences · 2026Review
- Villin like suppresses nasopharyngeal carcinoma proliferation by downregulating MYC.Scientific reports · 2025Article
- NamiRNA-Enhancer Network: The Changing Era Challenge and Chance of miRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- HBV sequence integrated to enhancer acting as oncogenic driver epigenetically promotes hepatocellular carcinoma development.Journal of experimental & clinical cancer research : CR · 2025Article
- Nuclear-activating miRNAs: unveiling the intricacies of subcellular miRNA function and regulation in cancer and immunity disease.Cancer cell international · 2025Review
- Easy triplex: An online tool for predicting the formation of DNA-RNA triple helices.Computational and structural biotechnology journal · 2025Article
- Epigenetic Modifiers in Cancer Metastasis.Biomolecules · 2024Review
- Nuclear miRNAs as transcriptional regulators in processes related to various cancers (Review).International journal of oncology · 2024Review
- miR-1246 promotes osteosarcoma cell migration via NamiRNA-enhancer network dependent on Argonaute 2.MedComm · 2024Article
- Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is one of the most malignant epithelial tumors. Studies have suggested that DNA hypermethylation of promoters and abnormal histone modifications could induce tumor suppressor genes (TSGs) downregulation in NSCLC. However, the exact mechanism of TSGs downregulation remains unclear. In this study, we found that there is no difference in the regions of most TSGs promoters in NSCLC. Moreover, we found that there is no DNA methylation difference in the region of VILL promoter in NSCLC compared with adjacent tissue samples by pyrosequencing. We further demonstrated that VILL was markedly reactivated in A549 and H1703 cells infected with miR-26A1 lentivirus while this activation was inhibited by JQ1, an enhancer inhibitor. In addition, we identified that miR-26A1 could function as a tumor suppressor to inhibit proliferation and metastasis of NSCLC cells. Chromatin immunoprecipitation assays revealed that overexpression of miR-26A1 could significantly induce the enrichment of H3K27ac at the enhancer regions in A549 cells. To sum up, our findings revealed that enhancer-mediated TSGs regulation occured in NSCLC, suggesting that miR-26A1 could serve as a key regulator and may be a potential therapeutic target for NSCLC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.