ArticleBritish journal of cancer2014
G-CSF and G-CSFR are highly expressed in human gastric and colon cancers and promote carcinoma cell proliferation and migration.
Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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Who cites it
77 citing papers in PubMed, 110 citations in OpenAlex.
- Article
- G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.European journal of medical research · 2026Article
- Recruitment of neutrophils by granulocyte colony-stimulating factor in cancer patients undergoing immunotherapy: the good, the bad, and the unknown.Frontiers in immunology · 2026Review
- Tuning of G-CSFR signaling by de novo-designed agonists.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- Epithelial Regnase-1 inhibits colorectal tumor growth by regulating IL-17 signaling via degradation ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Neutrophil extracellular traps and cannabinoids: potential in cancer metastasis.Frontiers in oncology · 2025Review
- Article
- Transcriptomic Profiling of Carboplatin- and Paclitaxel-Resistant Lung Adenocarcinoma Cells RevealsCurrent issues in molecular biology · 2024Article
- A strategy to design protein-based antagonists against type I cytokine receptors.PLoS biology · 2024Article
- Tumor-associated mesenchymal stromal cells modulate macrophage phagocytosis in stromal-rich colorectal cancer via PD-1 signaling.iScience · 2024Article
- Review
- Prediction of the survival status and tumor microenvironment in colorectal cancer through genotyping analysis based on toll-like receptors.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2024Article
- Long-term follow-up of cancer and catastrophic diseases in hematopoietic stem cell donors: a comprehensive matched cohort study.Bone marrow transplantation · 2024Article
- An immune-competent human gut microphysiological system enables inflammation-modulation by Faecalibacterium prausnitzii.NPJ biofilms and microbiomes · 2024Article
- Causal links between circulatory inflammatory cytokines and risk of digestive polyps: a Mendelian randomization analysis.Frontiers in pharmacology · 2024Article
- An immune-competent human gut microphysiological system enables inflammation-modulation ofResearch square · 2023Article
- Article
- G-CSF Is a Novel Mediator of T-Cell Suppression and an Immunotherapeutic Target for Women with Colon Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGranulocyte colony-stimulating factor (G-CSF) is a pro-inflammatory cytokine that stimulates myeloid stem cell maturation, proliferation, and migration into circulation. Despite being a known growth factor, the impact of G-CSF on solid tumours has not been well examined. G-CSF receptor (G-CSFR) is expressed by some tumours, and thus the aim of this study was to examine the expression and impact of G-CSF and G-CSFR on gastrointestinal tumours.
methodsIn this study, G-CSF expression was examined in human gastric and colon tumours and by tumour-derived stromal myofibroblasts and carcinoma cells. G-CSFR expression was examined on carcinoma cells isolated from human tissues. The effects of G-CSF on gastric and colon carcinoma cell proliferation, migration, and signalling were examined.
resultsG-CSFR was highly expressed in 90% of human gastric and colon carcinomas. G-CSF was also found to be highly produced by stromal myofibroblasts and carcinoma cells. Exposure of carcinoma cells to G-CSF led to increased proliferation and migration, and expansion of a sub-population of carcinoma cells expressing stem-like markers. These processes were dependent on ERK1/2 and RSK1 phosphorylation.
conclusionsThese data suggest that the G-CSF/R axis promotes gastric and colorectal cancer development and suggest they are potential tumour targets.
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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.