ArticleBritish journal of cancer1999
Granulocyte, granulocyte-macrophage, and macrophage colony-stimulating factors can stimulate the invasive capacity of human lung cancer cells.
Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 87 citations in OpenAlex.
- Understanding the dual role of granulocyte-macrophage colony-stimulating factor in the lung cancer tumor microenvironment and its therapeutic implications.Translational lung cancer research · 2026Review
- Comparative evaluation of immunomodulatory cytokines for oncolytic therapy based on a high-efficient platform for oHSV1 reconstruction.Virology journal · 2025Article
- Effect of colony‑stimulating factor in the mechanism of bone metastasis development (Review).Oncology reports · 2024Review
- Disrupting Smad3 potentiates immunostimulatory function of NK cells against lung carcinoma by promoting GM-CSF production.Cellular and molecular life sciences : CMLS · 2024Article
- Immune Evasion of G-CSF and GM-CSF in Lung Cancer.Tuberculosis and respiratory diseases · 2024Article
- Novel immunotherapeutic options for BCG-unresponsive high-risk non-muscle-invasive bladder cancer.Cancer medicine · 2023Review
- Article
- Myeloid-derived suppressor cells promote epithelial ovarian cancer cell stemness by inducing the CSF2/p-STAT3 signalling pathway.The FEBS journal · 2020Article
- Suppression of CXCL-1 Could Restore Necroptotic Pathway in Chronic Lymphocytic Leukemia.OncoTargets and therapy · 2020Article
- An epithelial-to-mesenchymal transition-inducing potential of granulocyte macrophage colony-stimulating factor in colon cancer.Scientific reports · 2017Article
- Stimulatory versus suppressive effects of GM-CSF on tumor progression in multiple cancer types.Experimental & molecular medicine · 2016Review
- Interleukin 4, interleukin 6 and osteopontin-serological markers of head and neck malignancy in primary diagnostics: A pilot study.Oncology letters · 2014Article
- Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells.Autophagy · 2014Article
- GM-CSF enhances tumor invasion by elevated MMP-2, -9, and -26 expression.Cancer medicine · 2013Article
- Development of a rapid streptavidin capture-based assay for the tyrosine phosphorylated CSF-1R in peripheral blood mononuclear cells.International journal of biological sciences · 2013Article
- Serum macrophage colony-stimulating factor (M-CSF) in patients with Hodgkin lymphoma.Medical oncology (Northwood, London, England) · 2012Article
- Synergistic effect of SCF and G-CSF on stem-like properties in prostate cancer cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Prognostic impact of CD57, CD68, M-CSF, CSF-1R, Ki67 and TGF-beta in soft tissue sarcomas.BMC clinical pathology · 2012Article
- uPA and uPAR shRNA inhibit angiogenesis via enhanced secretion of SVEGFR1 independent of GM-CSF but dependent on TIMP-1 in endothelial and glioblastoma cells.Molecular oncology · 2012Article
- Pleomorphic carcinoma of the lung producing granulocyte colony-stimulating factor: report of a case.Surgery today · 2011Article
Corrections and comments
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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
We and other researchers have previously found that colony-stimulating factors (CSFs), which generally include granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF), promote invasion by lung cancer cells. In the present study, we studied the effects of these CSFs on gelatinase production, urokinase plasminogen activator (uPA) production and their activity in human lung cancer cells. Gelatin zymographs of conditioned media derived from human lung adenocarcinoma cell lines revealed two major bands of gelatinase activity at 68 and 92 kDa, which were characterized as matrix metalloproteinase (MMP)-2 and MMP-9 respectively. Treatment with CSFs increased the 68- and 92-kDa activity and converted some of a 92-kDa proenzyme to an 82-kDa enzyme that was consistent with an active form of the MMP-9. Plasminogen activator zymographs of the conditioned media from the cancer cells showed that CSF treatment resulted in an increase in a 48-55 kDa plasminogen-dependent gelatinolytic activity that was characterized as human uPA. The conditioned medium from the cancer cells treated with CSFs stimulated the conversion of plasminogen to plasmin, providing a direct demonstration of the ability of enhanced uPA to increase plasmin-dependent proteolysis. The enhanced invasive behaviour of the cancer cells stimulated by CSFs was well correlated with the increase in MMPs and uPA activities. These data suggest that the enhanced production of extracellular matrix-degrading proteinases by the cancer cells in response to CSF treatment may represent a biochemical mechanism which promotes the invasive behaviour of the cancer cells.
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