ArticleInternational journal of chronic obstructive pulmonary disease2016
COPD promotes migration of A549 lung cancer cells: the role of chemokine CCL21.
Article in International journal of chronic obstructive pulmonary disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- An Ex Vivo Lung Histoculture Model for Studying Pulmonary Infection and Immune Response With SARS-CoV-2 as an Example of RNA Virus.Bio-protocol · 2025Article
- Bioinformatics and System Biology Approach to Reveal the Interaction Network and the Therapeutic Implications for Non-Small Cell Lung Cancer Patients With COVID-19.Frontiers in pharmacology · 2022Article
- Article
- Serum from patients with chronic obstructive pulmonary disease induces senescence-related phenotype in bronchial epithelial cells.Scientific reports · 2018Article
- Myocyte enhancer factor 2D provides a cross-talk between chronic inflammation and lung cancer.Journal of translational medicine · 2017Article
- Relationships between chronic obstructive pulmonary disease and lung cancer: biological insights.Journal of thoracic disease · 2016Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with COPD develop lung cancer more frequently than healthy smokers. At the same time, molecular mediators promoting various aspects of cancer cell progression are still elusive. In this report, we examined whether COPD can be coupled with increased migration of non-small-cell lung cancer cells A549 and, if so, whether this effect may be related to altered production and activity of chemokines CCL21, CXCL5, and CXCL12. The study showed that the migration of A549 cells through the polycarbonate membrane and basement membrane extract toward a chemotactic gradient elicited by serum from patients with COPD was markedly higher as compared with serum from healthy donors. The concentration of CCL21 and CXCL12, but not CXCL5, in serum from patients with COPD was also increased. Experiments in which CCL21- and CXCL12-dependent signaling was blocked revealed that increased migration of the cancer cells upon treatment with serum from patients with COPD was mediated exclusively by CCL21. Collectively, our results indicate that COPD may contribute to the progression of lung cancer via CCL21-dependent intensification of cancer cell migration.
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