ArticlePloS one2014
Chronic macrophage migration inhibitory factor exposure induces mesenchymal epithelial transition and promotes gastric and colon cancers.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- A PDGFRB-CD44-MIF crosstalk promotes cancer-associated cellular phenotypes in ATRT-TYR/MYC cell lines.Frontiers in oncology · 2026Article
- Targeting macrophage migration inhibitory factor as a potential therapeutic strategy in colorectal cancer.Oncogenesis · 2025Article
- Macrophage Migration Inhibitory Factor (MIF) and D-Dopachrome Tautomerase (DDT): Pathways to Tumorigenesis and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- CD74 Promotes a Pro-Inflammatory Tumor Microenvironment by Inducing S100A8 and S100A9 Secretion in Pancreatic Cancer.International journal of molecular sciences · 2023Article
- TA-MSCs, TA-MSCs-EVs, MIF: their crosstalk in immunosuppressive tumor microenvironment.Journal of translational medicine · 2022Review
- The Complex Network between Inflammation and Colorectal Cancer: A Systematic Review of the Literature.Cancers · 2021Review
- Article
- Hsp90-stabilized MIF supports tumor progression via macrophage recruitment and angiogenesis in colorectal cancer.Cell death & disease · 2021Article
- Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis.International journal of molecular sciences · 2020Review
- Dihydroartemisinin Regulates the Th/Treg Balance by Inducing Activated CD4+ T cell Apoptosis via Heme Oxygenase-1 Induction in Mouse Models of Inflammatory Bowel Disease.Molecules (Basel, Switzerland) · 2019Article
- Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer.Mediators of inflammation · 2019Article
- Macrophage migration inhibitory factor regulates mitochondrial dynamics and cell growth of human cancer cell lines through CD74-NF-κB signaling.The Journal of biological chemistry · 2018Article
- Neutralization of macrophage migration inhibitory factor improves host survival after Clostridium difficile infection.Anaerobe · 2018Article
- Isolation of CD 90+ Fibroblast/Myofibroblasts from Human Frozen Gastrointestinal Specimens.Journal of visualized experiments : JoVE · 2016Article
- A multi-targeted approach to suppress tumor-promoting inflammation.Seminars in cancer biology · 2015Review
- Prognostic value of several biomarkers for the patients with malignant pleural mesothelioma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Low-molecular-mass secretome profiling identifies HMGA2 and MIF as prognostic biomarkers for oral cavity squamous cell carcinoma.Scientific reports · 2015Article
- Stromal-dependent tumor promotion by MIF family members.Cellular signalling · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophage Migration Inhibitory Factor (MIF) is an inflammatory cytokine that is highly produced in gastrointestinal cancers. Since chronic inflammation is a risk factor for tumorigenesis in these cancers, in this study, the role of MIF in pro-tumorigenic events was examined. MIF and its receptor, CD74, were examined in gastric and colon tumors and found to be increased in most tumors with significantly higher expression in tumors from patients with lymph node metastasis. MIF was also found to be highly produced by cancer associated fibroblasts isolated from human tumors compared to fibroblasts from matched normal tissues from uninvolved areas. Fibroblast-produced MIF highly increased GI cancer cell proliferation, which was decreased upon neutralizing MIF or CD74. Chronic MIF treatment led to sustained proliferation and signaling events in non-transformed GI fibroblast cells, which was maintained upon removing MIF treatment for 8 weeks. Additionally, chronic treatment of normal GI cells expressing fibroblast markers for up to 16 weeks with MIF led to a drastic decrease of fibroblast markers with concurrent increase of epithelial markers. Transformation was examined by telomerase and focus forming assays. These results suggest the MIF promotes mesenchymal epithelial transition, cell transformation and tumorigenesis in GI cancers, and thus may be an important link between chronic inflammation and tumorigenesis.
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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.