ArticleFree radical biology & medicine2012
Cigarette smoke extract stimulates epithelial-mesenchymal transition through Src activation.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The trial behind it
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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- CNTN-1 regulates malignant biological behaviors of lung squamous cell carcinoma (LUSC) via the endoplasmic reticulum stress (ERS)/epithelial-mesenchymal transition (EMT) axis.Translational cancer research · 2026Article
- Clinicopathological Significance of Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- cAMP-PDE signaling in COPD: Review of cellular, molecular and clinical features.Biochemistry and biophysics reports · 2023Review
- DNA Damage and Oxidative Stress of Tobacco Smoke Condensate in Human Bladder Epithelial Cells.Chemical research in toxicology · 2022Article
- Hydrogen Sulfide Inhibits Bronchial Epithelial Cell Epithelial Mesenchymal Transition Through Regulating Endoplasm Reticulum Stress.Frontiers in molecular biosciences · 2022Article
- Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.International journal of molecular sciences · 2021Article
- The antioxidant N-acetylcysteine promotes immune response and inhibits epithelial-mesenchymal transition to alleviate pulmonary fibrosis in chronic obstructive pulmonary disease by suppressing the VWF/p38 MAPK axis.Molecular medicine (Cambridge, Mass.) · 2021Article
- Effects of cigarette smoke extract on bronchial epithelial cells stimulated with Cryptococcus neoformans.Medical microbiology and immunology · 2021Article
- Regulatory function of peroxiredoxin I on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung cancer development.Oncology letters · 2021Review
- Pivotal Role of Fyn Kinase in Parkinson's Disease and Levodopa-Induced Dyskinesia: a Novel Therapeutic Target?Molecular neurobiology · 2021Review
- TAp63α Is Involved in Tobacco Smoke-Induced Lung Cancer EMT and the Anti-cancer Activity of Curcumin via miR-19 Transcriptional Suppression.Frontiers in cell and developmental biology · 2021Article
- Effects of Inhaled Tobacco Smoke on the Pulmonary Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- The effects of cigarette smoking extracts on cell cycle and tumor spread: novel evidence.Future science OA · 2019Review
- The interplay of reactive oxygen species and the epidermal growth factor receptor in tumor progression and drug resistance.Journal of experimental & clinical cancer research : CR · 2018Review
- Targeting focal adhesion kinase overcomes erlotinib resistance in smoke induced lung cancer by altering phosphorylation of epidermal growth factor receptor.Oncoscience · 2018Article
- Melatonin suppresses fibrotic responses induced by cigarette smoke via downregulation of TGF-β1.Oncotarget · 2017Article
- Review
- Pine bark extract (Pycnogenol®) suppresses cigarette smoke-induced fibrotic response via transforming growth factor-β1/Smad family member 2/3 signaling.Laboratory animal research · 2017Article
- Cigarette smoke extract induces the epithelial-to-mesenchymal transitionToxicology research · 2017Article
- Role of AP-1 in the tobacco smoke-induced urocystic abnormal cell differentiation and epithelial-mesenchymal transitionInternational journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of lung fibrosis and cancer metastasis, two conditions associated with cigarette smoke (CS). CS has been reported to promote the EMT process. CS is the major cause of lung cancer and nearly half of lung cancer patients are active smokers. Nonetheless, the mechanism whereby CS induces EMT remains largely unknown. In this study we investigated the induction of EMT by CS and explored the underlying mechanisms in the human non-small-cell lung carcinoma (H358) cell line. We demonstrate that exposure to an extract of CS (CSE) decreases E-cadherin and increases N-cadherin and vimentin, markers of EMT, in H358 cells cultured in RPMI 1640 medium with 1% fetal bovine serum. Pretreatment with N-acetylcysteine (NAC), a potent antioxidant and precursor of glutathione, abrogated changes in these EMT markers. In addition, CSE activated Src kinase (shown as increased phosphorylation of Src at Tyr418), and the Src kinase inhibitor PP2 inhibited CS-stimulated EMT changes, suggesting that Src is critical in CSE-stimulated EMT induction. Furthermore, NAC treatment abrogated CSE-stimulated Src activation. However, co-incubation with catalase had no effect on CSE-mediated Src activation. Finally, acrolein, an unsaturated aldehyde present in CSE, caused Src activation. Taken together, these data suggest that CSE initiates EMT through Src, which is activated by CS through redox modification.
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Registered trials
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.