ArticleInternational journal of chronic obstructive pulmonary disease2023
Mettl3 Mediated m6A Methylation Involved in Epithelial-Mesenchymal Transition by Targeting SOCS3/STAT3/SNAI1 in Cigarette Smoking-Induced COPD.
Article in International journal of chronic obstructive pulmonary disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting METTL3/m6A/SOCS3 axis reprograms tumor-associated macrophage polarization to potentiate the efficacy of anti-PD-1 therapy in multiple myeloma.Cellular and molecular life sciences : CMLS · 2026Article
- Epitranscriptomics, immunometabolism, and NETosis: unlocking novel mechanisms of traditional Chinese medicine in COPD.Frontiers in immunology · 2026Review
- The role of OTUD1-mediated deubiquitination in disease pathogenesis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- METTL3 mediates m6A methylation of LCN2 through IGF2BP3 to promote ferroptosis in chronic obstructive pulmonary disease.Hereditas · 2025Article
- The Emerging Role of METTL3 in Lung Diseases.International journal of molecular sciences · 2025Review
- Decoding the role of mNeurochemistry international · 2025Review
- METTL3‑mediated m6A methylation and its impact on OTUD1 expression in chronic obstructive pulmonary disease.Molecular medicine reports · 2025Article
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- METTL3 blocked the progression of diabetic retinopathy through m6A-modified SOX2.Open medicine (Warsaw, Poland) · 2025Article
- METTL3/IGF2BP2-Mediated m6A RNA Methylation Drives Alveolar Macrophage-Dependent Neutrophil Recruitment in Cigarette Smoke-Induced COPD.Journal of inflammation research · 2025Article
- The Correlation Analysis Between m6A Methylation Modification and Ferroptosis Induced by Cigarette Smoke in Human Bronchial Epithelium.Immunity, inflammation and disease · 2024Article
- Role of m6A Methylation Regulators in the Diagnosis and Subtype Classification of COPD Based on the GEO Database.Journal of cellular and molecular medicine · 2024Article
- Examining the evidence for mutual modulation between m6A modification and circular RNAs: current knowledge and future prospects.Journal of experimental & clinical cancer research : CR · 2024Review
- Epigenetic regulation of macrophage activation in chronic obstructive pulmonary disease.Frontiers in immunology · 2024Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Persistent inflammation and epithelial-mesenchymal transition are essential pathophysiological processes in chronic obstructive pulmonary disease (COPD) and involve airway remodeling. m6A methylation modification was discovered to play an important role in various diseases. Nevertheless, the regulatory role of m6A methylation has not yet been investigated in cigarette smoking-induced COPD. The study aims to explore the regulatory role of m6A methylation in cigarette smoking-induced COPD. Patients and Methods: In this study, two Gene Expression Omnibus (GEO) datasets were first utilized to analyze the expression profiles of m6A RNA methylation regulators in COPD. We then established a cell model of COPD by exposing human bronchial epithelial cells (HBECs) to cigarette smoke extract (CSE) in vitro and detected the expression of m6A writer Mettl3 and EMT phenotype markers. RNA interference, cycloleucine, RT-qPCR, western blot, MeRIP-sequencing, and cell migration assay were performed to investigate the potential effect of Mettl3 on the EMT process in CSE-induced HBECs. Results: Our results showed that Mettl3 expression was significantly elevated in cigarette smoking-induced COPD patients and in a cellular model of COPD. Furthermore, Mettl3 silence and cycloleucine treatment inhibited the EMT process of HBECs caused by CSE. Mechanically, Mettl3 silence weakens the m6A methylation of SOCS3 mRNA to enhance the protein expression of SOCS3, inhibiting CSE-induced SOCS3/STAT3/SNAI1 signaling and EMT processes in HBECs. Conclusion: Our study inferred that Mettl3-mediated m6A RNA methylation modification modulates CSE-induced EMT by targeting SOCS3 mRNA and ultimately serves as a crucial regulator in the emergence of COPD. This conclusion reinforces the regulatory role of m6A methylation in COPD.
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