ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Na,K-ATPase is a target of cigarette smoke and reduced expression predicts poor patient outcome of smokers with lung cancer.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- The role of Na,K‑ATPase in lung diseases (Review).Molecular medicine reports · 2025Review
- Novel Interleukin-11 Inhibitors Attenuate Collagen Production in Patient-Derived Synovial Fibroblasts.Cureus · 2025Article
- Tumour blood flow for prediction of human prostate cancer aggressiveness: a study with Rubidium-82 PET, MRI and NaEuropean journal of nuclear medicine and molecular imaging · 2021Article
- Evaluation of the Erythrocyte Membrane in Head and Neck Cancer Patients.The Journal of membrane biology · 2020Article
- Effects of Inhaled Tobacco Smoke on the Pulmonary Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- The impact of smoking status on radiologic tumor progression patterns and response to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors in lung adenocarcinoma with activating EGFR mutations.Journal of thoracic disease · 2016Article
- Article
- The biological and clinical effects of smoking by patients with cancer and strategies to implement evidence-based tobacco cessation support.The Lancet. Oncology · 2014Review
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Diminished Na,K-ATPase expression has been reported in several carcinomas and has been linked to tumor progression. However, few studies have determined whether Na,K-ATPase function and expression are altered in lung malignancies. Because cigarette smoke (CS) is a major factor underlying lung carcinogenesis and progression, we investigated whether CS affects Na,K-ATPase activity and expression in lung cell lines. Cells exposed to CS in vitro showed a reduction of Na,K-ATPase activity. We detected the presence of reactive oxygen species (ROS) in cells exposed to CS before Na,K-ATPase inhibition, and neutralization of ROS restored Na,K-ATPase activity. We further determined whether Na,K-ATPase expression correlated with increasing grades of lung adenocarcinoma and survival of patients with smoking history. Immunohistochemical analysis of lung adenocarcinoma tissues revealed reduced Na,K-ATPase expression with increasing tumor grade. Using tissue microarray containing lung adenocarcinomas of patients with known smoking status, we found that high expression of Na,K-ATPase correlated with better survival. For the first time, these data demonstrate that CS is associated with loss of Na,K-ATPase function and expression in lung carcinogenesis, which might contribute to disease progression.
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