ArticleAmerican journal of translational research2015
Cigarette smoking impairs the response of EGFR-TKIs therapy in lung adenocarcinoma patients by promoting EGFR signaling and epithelial-mesenchymal transition.
Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- 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
- First- or second-generation epidermal growth factor receptor tyrosine kinase inhibitors in a large, real-world cohort of patients with non-small cell lung cancer.Therapeutic advances in medical oncology · 2021Article
- Article
- Targeting PD-L1 in non-small cell lung cancer using CAR T cells.Oncogenesis · 2020Article
- High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis.Cancers · 2020Review
- miR‑146a‑5p targets TCSF and influences cell growth and apoptosis to repress NSCLC progression.Oncology reports · 2019Article
- EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies.Frontiers in oncology · 2019Review
- Advances in Molecular Mechanisms and Immunotherapy Involving the Immune Cell-Promoted Epithelial-to-Mesenchymal Transition in Lung Cancer.Journal of oncology · 2019Review
- Cumulative smoking dose affects the clinical outcomes of EGFR-mutated lung adenocarcinoma patients treated with EGFR-TKIs: a retrospective study.BMC cancer · 2018Article
- Role of Krüppel-like factor 4 in cigarette smoke-induced pulmonary vascular remodeling.American journal of translational research · 2018Article
- Water-pipe smoking promotes epithelial-mesenchymal transition and invasion of human breast cancer cells via ERK1/ERK2 pathways.Cancer cell international · 2018Article
- Targeting focal adhesion kinase overcomes erlotinib resistance in smoke induced lung cancer by altering phosphorylation of epidermal growth factor receptor.Oncoscience · 2018Article
- Real-World Data on Prognostic Factors for Overall Survival in EGFR Mutation-Positive Advanced Non-Small Cell Lung Cancer Patients Treated with First-Line Gefitinib.The oncologist · 2017Article
- Non-coding RNAs as emerging regulators of epithelial to mesenchymal transition in non-small cell lung cancer.Oncotarget · 2017Review
- Role of microRNA-21 in radiosensitivity in non-small cell lung cancer cells by targeting PDCD4 gene.Oncotarget · 2017Article
- Prostatic vascular damage induced by cigarette smoking as a risk factor for recovery after holmium laser enucleation of the prostate (HoLEP).Oncotarget · 2017Article
- Epithelial-to-mesenchymal transition correlates with gefitinib resistance in NSCLC cells and the liver X receptor ligand GW3965 reverses gefitinib resistance through inhibition of vimentin.OncoTargets and therapy · 2017Article
- Calpain 1 regulates TGF-β1-induced epithelial-mesenchymal transition in human lung epithelial cells via PI3K/Akt signaling pathway.American journal of translational research · 2017Article
- Epigenome-wide association study of smoking and DNA methylation in non-small cell lung neoplasms.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking represents for the highest risk-factor for non-small cell lung cancer (NSCLC), and a growing body of evidence suggested that smoking was associated with a high recurrence and poor therapeutic response of NSCLC as well. On the other hand, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs), such as gefitinib, has been proved to be an efficient and safe strategy for treating NSCLC. Although accumulating clinical data suggested that smoking history might influence the therapeutic effects of EGFR-TKIs even in NSCLC patients harboring sensitive EGFR mutation, the exact effects of cigarette smoking on the efficacy of EGFR-TKIs treatment in NSCLC patients remain exclusive. In this study, we firstly identified the adverse effect of smoking exposure on the efficacy of EGFR-TKIs treatment against lung adenocarcinoma in mutation-positive patients by retrospective analysis of clinical data. The hypo-responsiveness of smoking patients on the therapy was accompanied with persistent activation of EGFR-downstream signal molecules ERK1/2 and AKT, which could not be inhibited by gefitinib and thus lead to the failure of EGFR-TKIs treatment. Based on our in vitro data, it was also found that long-term cigarette smoking extract (CSE) exposure induced epithelial-mesenchymal transition (EMT), which might also contribute to acquired resistance to EGFR-TKIs. Taken together, our findings suggested that cigarette smoking negatively regulated the clinical outcome of EGFR-TKIs therapy in lung adenocarcinoma patients, which was correlated with the activation of EGFR signaling and the induction of EMT.
Indexed as
Identifiers
26692946PMC4656779W2221644116What OpenQuestion holds
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.