ArticleRespiratory research2021
FERMT3 mediates cigarette smoke-induced epithelial-mesenchymal transition through Wnt/β-catenin signaling.
Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- A Chemoenzymatic Method To Systematically Quantify Core Fucosylation Stoichiometry of Glycoproteins and Reveal Its Roles in EMT and Embryonic Development.Analytical chemistry · 2026Article
- Exploratory CT-Based Assessment of Emphysema Burden in Smokers with Bipolar Disorder Receiving Lithium Treatment.International journal of chronic obstructive pulmonary disease · 2026Observational
- LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway.International journal of chronic obstructive pulmonary disease · 2026Article
- Exploring the Roles of Wnt Signaling Pathway and Non-Coding RNAs in COPD.International journal of chronic obstructive pulmonary disease · 2026Review
- Molecular signatures under hexavalent chromium, particulate matter 2.5, and cigarette smoking exposures.Discover oncology · 2025Article
- Integrative analysis identifies FERMT3 as a key regulator of metabolic reprogramming in keloid scarring and metabolic syndrome.Functional & integrative genomics · 2025Article
- TRIB1 facilitates the proliferation and migration of ovarian cancer cells by inducing EMT progression.Histology and histopathology · 2025Article
- Medwakh smoking induces alterations in salivary proteins and cytokine expression: a clinical exploratory proteomics investigation.Clinical proteomics · 2025Article
- METTL3/IGF2BP2-Mediated m6A RNA Methylation Drives Alveolar Macrophage-Dependent Neutrophil Recruitment in Cigarette Smoke-Induced COPD.Journal of inflammation research · 2025Article
- Airway remodeling in chronic obstructive pulmonary disease: characteristics and opportunities.Frontiers in medicine · 2025Review
- PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- MiR-125b-5p alleviates pulmonary fibrosis by inhibiting TGFβ1-mediated epithelial-mesenchymal transition via targeting BAK1.Respiratory research · 2024Article
- Review
- Analysis of network expression and immune infiltration of disulfidptosis-related genes in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2024Article
- MiR-23a-5p alleviates chronic obstructive pulmonary disease through targeted regulation of RAGE-ROS pathway.Respiratory research · 2024Article
- SHP-1 mediates cigarette smoke extract-induced epithelial-mesenchymal transformation and inflammation in 16HBE cells.Open medicine (Warsaw, Poland) · 2024Article
- CSE triggers ferroptosis via SIRT4-mediated GNPAT deacetylation in the pathogenesis of COPD.Respiratory research · 2023Article
- Keratin 15 protects against cigarette smoke-induced epithelial mesenchymal transformation by MMP-9.Respiratory research · 2023Article
- Mechanistic Regulation of Wnt Pathway-Related Progression of Chronic Obstructive Pulmonary Disease Airway Lesions.International journal of chronic obstructive pulmonary disease · 2023Review
- Hesperidin inhibits tobacco smoke-induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway.Oncology letters · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial-mesenchymal transition (EMT) is an essential pathophysiological process in COPD and plays an important role in airway remodeling, fibrosis, and malignant transformation of COPD. Previous studies have indicated FERMT3 is downregulated and plays a tumor-suppressive role in lung cancer. However, the role of FERMT3 in COPD, including EMT, has not yet been investigated.
methodsThe present study aimed to explore the potential role of FERMT3 in COPD and its underlying molecular mechanisms. Three GEO datasets were utilized to analyse FERMT3 gene expression profiles in COPD. We then established EMT animal models and cell models through cigarette smoke (CS) or cigarette smoke extract (CSE) exposure to detect the expression of FERMT3 and EMT markers. RT-PCR, western blot, immunohistochemical, cell migration, and cell cycle were employed to investigate the potential regulatory effect of FERMT3 in CSE-induced EMT.
resultsBased on Gene Expression Omnibus (GEO) data set analysis, FERMT3 expression in bronchoalveolar lavage fluid was lower in COPD smokers than in non-smokers or smokers. Moreover, FERMT3 expression was significantly down-regulated in lung tissues of COPD GOLD 4 patients compared with the control group. Cigarette smoke exposure reduced the FERMT3 expression and induces EMT both in vivo and in vitro. The results showed that overexpression of FERMT3 could inhibit EMT induced by CSE in A549 cells. Furthermore, the CSE-induced cell migration and cell cycle progression were reversed by FERMT3 overexpression. Mechanistically, our study showed that overexpression of FERMT3 inhibited CSE-induced EMT through the Wnt/β-catenin signaling.
conclusionsIn summary, these data suggest FERMT3 regulates cigarette smoke-induced epithelial-mesenchymal transition through Wnt/β-catenin signaling. These findings indicated that FERMT3 was correlated with the development of COPD and may serve as a potential target for both COPD and lung cancer.
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