ArticleCancer prevention research (Philadelphia, Pa.)2012
Smoking attenuates transforming growth factor-β-mediated tumor suppression function through downregulation of Smad3 in lung cancer.
Article in Cancer prevention research (Philadelphia, Pa.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- Smoking and endometriosis: A narrative review.Tobacco induced diseases · 2025Review
- Alcohol, Smoking, and Risks of Breast Cancer Recurrence and Mortality among Women with Luminal, Triple-Negative, and HER2-Overexpressing Breast Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024Article
- Looking at the Data on Smoking and Post-COVID-19 Syndrome-A Literature Review.Journal of personalized medicine · 2024Review
- Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells.Tobacco induced diseases · 2023Article
- Clinical and Histopathological Factors Associated with the Tumoral Expression of TGF-Advances in preventive medicine · 2022Article
- Epigenetic Reprogramming of Tumor-Associated Fibroblasts in Lung Cancer: Therapeutic Opportunities.Cancers · 2021Review
- Integrated TCGA and GEO analysis showed that SMAD7 is an independent prognostic factor for lung adenocarcinoma.Medicine · 2020Article
- Review
- The role of contextual signal TGF-β1 inducer of epithelial mesenchymal transition in metastatic lung adenocarcinoma patients with brain metastases: an update on its pathological significance and therapeutic potential.Contemporary oncology (Poznan, Poland) · 2019Review
- Investigating the mechanism by which SMAD3 induces PAX6 transcription to promote the development of non-small cell lung cancer.Respiratory research · 2018Article
- Article
- Decrease of FSTL1-BMP4-Smad signaling predicts poor prognosis in lung adenocarcinoma but not in squamous cell carcinoma.Scientific reports · 2017Article
- Aberrant DNA methylation in non-small cell lung cancer-associated fibroblasts.Carcinogenesis · 2015Article
- Tobacco smoking is associated with methylation of genes related to coronary artery disease.Clinical epigenetics · 2015Article
- The biological and clinical effects of smoking by patients with cancer and strategies to implement evidence-based tobacco cessation support.The Lancet. Oncology · 2014Review
- A genome-wide gene-environment interaction analysis for tobacco smoke and lung cancer susceptibility.Carcinogenesis · 2014Article
- Nicotine-mediated cell proliferation and tumor progression in smoking-related cancers.Molecular cancer research : MCR · 2014Review
- Tumors as organs: biologically augmenting radiation therapy by inhibiting transforming growth factor β activity in carcinomas.Seminars in radiation oncology · 2013Review
- Role of TGF-β signaling in curcumin-mediated inhibition of tumorigenicity of human lung cancer cells.Journal of cancer research and clinical oncology · 2013Article
- Smoking induces epithelial-to-mesenchymal transition in non-small cell lung cancer through HDAC-mediated downregulation of E-cadherin.Molecular cancer therapeutics · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiologic studies have shown that most cases of lung cancers (85%-90%) are directly attributable to cigarette smoking. Although much information has been gained about the effects of cigarette smoking on various signaling pathways causing lung cancer, nothing is known about the effect of cigarette smoking on the TGF-β-induced tumor suppressor function in lung cancer. To address this issue, lung adenocarcinoma A549 and immortalized bronchial epithelial HPL1A cells were chronically treated with cigarette smoke condensate (CSC) and dimethyl sulfoxide (as a control) to mimic the conditions of long-term cigarette smoking. Prolonged exposure of these cells to CSC resulted in a decrease in Smad3 and Smad4 complex formation and TGF-β-mediated transcription due to reduced expression of Smad3. Long-term CSC treatment reduced apoptosis, increased cell viability, decreased TGF-β-mediated growth inhibition, and enhanced tumorigenicity. The decrease in apoptosis is due to the upregulation of Bcl-2, which is a downstream target of Smad3. Re-expression of Smad3 in the CSC-treated cells restored TGF-β signaling, increased apoptosis, and decreased cell viability and tumorigenicity. Withdrawal of CSC treatment resulted in the restoration of Smad3 expression, reduction in cell viability, and increased TGF-β-mediated growth inhibition. Expression of Smad3 is lower in lung tumors of current smokers than that observed in never-smokers. Collectively, these data provide evidence that cigarette smoking promotes tumorigenicity partly by abrogating TGF-β-mediated growth inhibition and apoptosis by reducing expression of Smad3.
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