ArticleAmerican journal of respiratory cell and molecular biology2014
Cigarette smoke activates the proto-oncogene c-src to promote airway inflammation and lung tissue destruction.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis.The European respiratory journal · 2024Pooled it
- CXCL11 levels regulate lung Treg responses to deter the onset of HIV-related COPD.Respiratory research · 2026Article
- UHPLC -Q-Orbitrap HRMS Integrated with Network Pharmacology Reveals the Anti-COPD Mechanism of Jianzhong Peiyuan Decoction and Functional Validation of Core Component Luteolin.Journal of inflammation research · 2026Article
- Analysis of the effects of perfluorooctane sulfonate on COPD using network toxicology and molecular docking.iScience · 2025Article
- Bioinformatics identification of mitochondria and macrophage polarization-related genes in COPD and their potential mechanisms.Frontiers in immunology · 2025Article
- Cigarette smoke alters calcium flux to induce PP2A membrane trafficking and endothelial cell permeability.Scientific reports · 2024Article
- The paradox of the safer cigarette: understanding the pulmonary effects of electronic cigarettes.The European respiratory journal · 2024Review
- Analysis of Communal Molecular Mechanism Between Chronic Obstructive Pulmonary Disease and Osteoporosis.International journal of chronic obstructive pulmonary disease · 2023Article
- Airway basal cells show a dedifferentiated KRT17Nature communications · 2022Article
- Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo.Antioxidants (Basel, Switzerland) · 2022Article
- Structural alteration of lung parenchyma in patients with NF1: a phenotyping study using multidetector computed tomography (MDCT).Orphanet journal of rare diseases · 2021Article
- Cigarette smoke induction of S100A9 contributes to chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Targeting c-Src Reverses Accelerated GPX-1 mRNA Decay in Chronic Obstructive Pulmonary Disease Airway Epithelial Cells.American journal of respiratory cell and molecular biology · 2020Article
- Chronic Cigarette Smoke Exposure Subdues PP2A Activity by Enhancing Expression of the Oncogene CIP2A.American journal of respiratory cell and molecular biology · 2018Article
- The Importance of Tyrosine Phosphorylation Control of Cellular Signaling Pathways in Respiratory Disease: pY and pY Not.American journal of respiratory cell and molecular biology · 2018Review
- Phospholipid transfer protein and alpha-1 antitrypsin regulate Hck kinase activity during neutrophil degranulation.Scientific reports · 2018Article
- Lignans Isolated From Flower Buds ofFrontiers in pharmacology · 2018Article
- p66Shc Mediates Mitochondrial Dysfunction Dependent on PKC Activation in Airway Epithelial Cells Induced by Cigarette Smoke.Oxidative medicine and cellular longevity · 2018Article
- The role of Src & ERK1/2 kinases in inspiratory resistive breathing induced acute lung injury and inflammation.Respiratory research · 2017Article
- Prioritizing chronic obstructive pulmonary disease (COPD) candidate genes in COPD-related networks.Oncotarget · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The diagnosis of chronic obstructive pulmonary disease (COPD) confers a 2-fold increased lung cancer risk even after adjusting for cigarette smoking, suggesting that common pathways are operative in both diseases. Although the role of the tyrosine kinase c-Src is established in lung cancer, less is known about its impact in other lung diseases, such as COPD. This study examined whether c-Src activation by cigarette smoke contributes to the pathogenesis of COPD. Cigarette smoke increased c-Src activity in human small airway epithelial (SAE) cells from healthy donors and in the lungs of exposed mice. Similarly, higher c-Src activation was measured in SAE cells from patients with COPD compared with healthy control subjects. In SAE cells, c-Src silencing or chemical inhibition prevented epidermal growth factor (EGF) receptor signaling in response to cigarette smoke but not EGF stimulation. Further studies showed that cigarette smoke acted through protein kinase C α to trigger c-Src to phosphorylate EGF receptor and thereby to induce mitogen-activated protein kinase responses in these cells. To further investigate the role of c-Src, A/J mice were orally administered the specific Src inhibitor AZD-0530 while they were exposed to cigarette smoke for 2 months. AZD-0530 treatment blocked c-Src activation, decreased macrophage influx, and prevented airspace enlargement in the lungs of cigarette smoke-exposed mice. Moreover, inhibiting Src deterred the cigarette smoke-mediated induction of matrix metalloproteinase-9 and -12 in alveolar macrophages and lung expression of cathepsin K, IL-17, TNF-α, MCP-1, and KC, all key factors in the pathogenesis of COPD. These results indicate that activation of the proto-oncogene c-Src by cigarette smoke promotes processes linked to the development of COPD.
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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.