ArticleFrontiers in physiology2013
Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN.
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- The Anti-EMMPRIN Monoclonal Antibody hMR18-mAb Induces Tumor Dormancy and Inhibits the EMT Process in Human Carcinoma Cell Lines Co-Cultured with Macrophages.Biomedicines · 2025Article
- EMMPRIN Correlated with β-CATENIN in Various t Stages of Colorectal Adenocarcinoma.Asian Pacific journal of cancer prevention : APJCP · 2025Observational
- p53 at the crossroads of tumor immunity.Nature cancer · 2024Review
- Glucose Promotes EMMPRIN/CD147 and the Secretion of Pro-Angiogenic Factors in a Co-Culture System of Endothelial Cells and Monocytes.Biomedicines · 2024Article
- EMMPRIN promotes spheroid organization and metastatic formation: comparison between monolayers and spheroids of CT26 colon carcinoma cells.Frontiers in immunology · 2024Article
- Soluble CD147 regulates endostatin via its effects on the activities of MMP-9 and secreted proteasome 20S.Frontiers in immunology · 2024Article
- CCL16 is a pro-tumor chemokine that recruits monocytes and macrophages to promote hepatocellular carcinoma progression.American journal of cancer research · 2024Article
- CD147 promotes breast cancer migration and invasion by inducing epithelial-mesenchymal transition via the MAPK/ERK signaling pathway.BMC cancer · 2023Article
- Combined Biomarker System Predicts Prognosis in Patients with Metastatic Oral Squamous Cell Carcinoma.Cancers · 2023Article
- Article
- TNF-α Secreted from Macrophages Increases the Expression of Prometastatic Integrin αV in Gastric Cancer.International journal of molecular sciences · 2022Article
- Article
- Mini-Review: Can the Metastatic Cascade Be Inhibited by Targeting CD147/EMMPRIN to Prevent Tumor Recurrence?Frontiers in immunology · 2022Review
- Loss of basigin expression in uterine cells leads to subfertility in female mice†.Biology of reproduction · 2021Article
- The role of EMMPRIN/CD147 in regulating angiogenesis in patients with psoriatic arthritis.Arthritis research & therapy · 2020Article
- P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020Review
- [Tumor-associated macrophages and hematologic malignancies].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018Article
- Function of miR-146a-5p in Tumor Cells As a Regulatory Switch between Cell Death and Angiogenesis: Macrophage Therapy Revisited.Frontiers in immunology · 2017Article
- CD147 and matrix-metalloproteinase-2 expression in metastatic and non-metastatic uveal melanomas.BMC ophthalmology · 2016Article
- Tumor-associated macrophages and extracellular matrix metalloproteinase inducer in prognosis of multiple myeloma.Leukemia · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor macrophages are generally considered to be alternatively/M2 activated to induce secretion of pro-angiogenic factors such as VEGF and MMPs. EMMPRIN (CD147, basigin) is overexpressed in many tumor types, and has been shown to induce fibroblasts and endothelial cell expression of MMPs and VEGF. We first show that tumor cell interactions with macrophages resulted in increased expression of EMMPRIN and induction of MMP-9 and VEGF. Human A498 renal carcinoma or MCF-7 breast carcinoma cell lines were co-cultured with the U937 monocytic-like cell line in the presence of TNFα (1 ng/ml). Membranal EMMPRIN expression was increased in the co-cultures (by 3-4-folds, p < 0.01), as was the secretion of MMP-9 and VEGF (by 2-5-folds for both MMP-9 and VEGF, p < 0.01), relative to the single cultures with TNFα. Investigating the regulatory mechanisms, we show that EMMPRIN was post-translationally regulated by miR-146a, as no change was observed in the tumoral expression of EMMPRIN mRNA during co-culture, expression of miR-146a was increased and its neutralization by its antagomir inhibited EMMPRIN expression. The secretion of EMMPRIN was also enhanced (by 2-3-folds, p < 0.05, only in the A498 co-culture) via shedding off of the membranal protein by a serine protease that is yet to be identified, as demonstrated by the use of wide range protease inhibitors. Finally, soluble EMMPRIN enhanced monocytic secretion of MMP-9 and VEGF, as inhibition of its expression levels by neutralizing anti-EMMPRIN or siRNA in the tumor cells lead to subsequent decreased induction of these two pro-angiogenic proteins. These results reveal a mechanism whereby tumor cell-macrophage interactions promote angiogenesis via an EMMPRIN-mediated pathway.
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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.