ArticleThe American journal of pathology2014
uPAR induces expression of transforming growth factor β and interleukin-4 in cancer cells to promote tumor-permissive conditioning of macrophages.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- UPR-CEBPB-MIF Signaling Links to Macrophage Polarization and an Immunosuppressive Tumor Microenvironment in Clear Cell Renal Cell Carcinoma.Annals of surgical oncology · 2026Article
- From in-silico QSAR modeling to in-vitro MTT assay: experimental validation of novel uPAR leads for triple-negative breast cancer (TNBC) and skin cancer.Scientific reports · 2026Article
- uPAR-directed immunotherapies in solid tumors: current advances and future perspectives.Frontiers in pharmacology · 2026Review
- Review
- Article
- uPAR (PLAUR) Marks Two Intra-Tumoral Subtypes of Glioblastoma: Insights from Single-Cell RNA Sequencing.International journal of molecular sciences · 2024Article
- Targeting circulating tumor cells to prevent metastases.Human cell · 2024Review
- Macrophages and Urokinase Plasminogen Activator Receptor System in Multiple Myeloma: Case Series and Literature Review.International journal of molecular sciences · 2023Review
- Targeting oral tumor microenvironment for effective therapy.Cancer cell international · 2023Review
- Article
- Circular RNA circWWC3 augments breast cancer progression through promoting M2 macrophage polarization and tumor immune escape via regulating the expression and secretion of IL-4.Cancer cell international · 2022Article
- Macrophages Are a Double-Edged Sword: Molecular Crosstalk between Tumor-Associated Macrophages and Cancer Stem Cells.Biomolecules · 2022Review
- The Urokinase Receptor (uPAR) as a "Trojan Horse" in Targeted Cancer Therapy: Challenges and Opportunities.Cancers · 2021Review
- Immune evasion by cancer stem cells.Regenerative therapy · 2021Review
- uPAR: An Essential Factor for Tumor Development.Journal of Cancer · 2021Review
- An individualized immune signature of pretreatment biopsies predicts pathological complete response to neoadjuvant chemoradiotherapy and outcomes in patients with esophageal squamous cell carcinoma.Signal transduction and targeted therapy · 2020Article
- Article
- High baseline soluble urokinase plasminogen activator receptor (suPAR) serum levels indicate adverse outcome after resection of pancreatic adenocarcinoma.Carcinogenesis · 2019Article
- LILRB4 signalling in leukaemia cells mediates T cell suppression and tumour infiltration.Nature · 2018Article
- Cancer immunotherapy with recombinant poliovirus induces IFN-dominant activation of dendritic cells and tumor antigen-specific CTLs.Science translational medicine · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cells condition macrophages and other inflammatory cells in the tumor microenvironment so that these cells are more permissive for cancer growth and metastasis. Conditioning of inflammatory cells reflects, at least in part, soluble mediators (such as transforming growth factor β and IL-4) that are released by cancer cells and alter the phenotype of cells of the innate immune system. Signaling pathways in cancer cells that potentiate this activity are incompletely understood. The urokinase receptor (uPAR) is a cell-signaling receptor known to promote cancer cell survival, proliferation, metastasis, and cancer stem cell-like properties. The present findings show that uPAR expression in diverse cancer cells, including breast cancer, pancreatic cancer, and glioblastoma cells, promotes the ability of these cells to condition co-cultured bone marrow-derived macrophages so that the macrophages express significantly increased levels of arginase 1, a biomarker of the alternatively activated M2 macrophage phenotype. Expression of transforming growth factor β was substantially increased in uPAR-expressing cancer cells via a mechanism that requires uPA-initiated cell signaling. uPAR also controlled expression of IL-4 in cancer cells via a mechanism that involves activation of ERK1/2. The ability of uPAR to induce expression of factors that condition macrophages in the tumor microenvironment may constitute an important mechanism by which uPAR promotes cancer progression.
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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.