ArticleMolecular cancer therapeutics2012
Smoking induces epithelial-to-mesenchymal transition in non-small cell lung cancer through HDAC-mediated downregulation of E-cadherin.
Article in Molecular cancer therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 86 citations in OpenAlex.
- Multi-omics analysis and functional validation of CHEK1 as an independent prognostic biomarker in Pancreatic cancer.PloS one · 2026Article
- Smoking induces different expression of miR-320b and miR-10b-5p in plasma extracellular vesicles of non-small cell lung cancer patients.The journal of liquid biopsy · 2025Article
- Article
- Pathological mechanisms of cigarette smoking, dietary, and sedentary lifestyle risks in vascular dysfunction: mitochondria as a common target of risk factors.Pflugers Archiv : European journal of physiology · 2023Review
- Molecular Mechanisms and Risk Factors Related to the Pathogenesis of Peyronie's Disease.International journal of molecular sciences · 2023Review
- DNA Damage and Oxidative Stress of Tobacco Smoke Condensate in Human Bladder Epithelial Cells.Chemical research in toxicology · 2022Article
- Regulation of epithelial-mesenchymal transition by protein lysine acetylation.Cell communication and signaling : CCS · 2022Review
- Review
- Histone deacetylases modulate resistance to the therapy in lung cancer.Frontiers in genetics · 2022Review
- SATB1 protein is associated with the epithelial‑mesenchymal transition process in non‑small cell lung cancers.Oncology reports · 2021Article
- Review
- Circulating tumor cell analysis in locally advanced and metastatic squamous cell carcinoma of the head and neck.Laryngoscope investigative otolaryngology · 2020Article
- Artesunate inhibits epithelial-mesenchymal transition in non-small-cell lung cancer (NSCLC) cells by down-regulating the expression ofBioengineered · 2020Article
- Differential expression of lung adenocarcinoma transcriptome with signature of tobacco exposure.Journal of applied genetics · 2020Article
- Suppressing migration and invasion of H1299 lung cancer cells by honokiol through disrupting expression of an HDAC6-mediated matrix metalloproteinase 9.Food science & nutrition · 2020Article
- Genetically Engineered Lung Cancer Cells for Analyzing Epithelial-Mesenchymal Transition.Cells · 2019Article
- Transcriptomic and barrier responses of human airway epithelial cells exposed to cannabis smoke.Physiological reports · 2019Article
- Smoking affects gene expression in blood of patients with ischemic stroke.Annals of clinical and translational neurology · 2019Article
- Effect of asiatic acid on epithelial-mesenchymal transition of human alveolar epithelium A549 cells induced by TGF-β1.Oncology letters · 2019Article
- Tobacco smoking induces cardiovascular mitochondrial oxidative stress, promotes endothelial dysfunction, and enhances hypertension.American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Epidemiological studies have shown that most cases of lung cancers (85%-90%) are directly attributable to tobacco smoking. Although association between cigarette smoking and lung cancer is well documented, surprisingly little is known about the molecular mechanisms of how smoking is involved in epithelial-to-mesenchymal transition (EMT) through epigenetic changes. Here, we show that lung cancer patients with a smoking history have low E-cadherin levels and loss of E-cadherin is a poor prognostic factor in smokers. Moreover, the downregulation of E-cadherin correlates with the number of pack years. In an attempt to determine the role of long-term cigarette smoking on EMT, we observed that treatment of lung cell lines with cigarette smoke condensate (CSC) induces EMT through downregulation of epithelial markers, including E-cadherin and upregulation of mesenchymal markers. CSC decreases E-cadherin expression at the transcriptional level through upregulation of LEF1 and Slug, and knockdown of these two proteins increases E-cadherin expression. Importantly, chromatin immunoprecipitation assays suggest that LEF-1 and Slug binding to E-cadherin promoter is important for CSC-mediated downregulation of E-cadherin. The histone deacetylase (HDAC) inhibitor MS-275 reverses CSC-induced EMT, migration, and invasion through the restoration of E-cadherin expression. These results suggest that recruitment of HDACs by transcriptional repressors LEF-1 and Slug is responsible for E-cadherin suppression and EMT in cigarette smokers and provide a potential drug target toward the treatment of lung cancer.
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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.