ArticleBMC cancer2016
uPAR enhances malignant potential of triple-negative breast cancer by directly interacting with uPA and IGF1R.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Herbal Melanin Inhibits Colorectal Cancer Cell Motility, Invasiveness, and Epithelial-Mesenchymal Transition, Associated with u-PAR Downregulation Through JNK and ERK Pathways.Current issues in molecular biology · 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
- Emerging roles of haemostatic proteins as markers of disease progression and prognosis in breast cancer.Exploration of targeted anti-tumor therapy · 2026Review
- Review
- Highly Adaptable Dendrimer Gel Nanoparticles with Dual Targeting of uPAR and Ribonucleotide Reductase R2 for Better Retention and Improved Therapeutic Outcomes in Triple-Negative Breast Cancer.ACS applied materials & interfaces · 2025Article
- Proteomics-Based Soluble Urokinase Plasminogen Activator Receptor Levels and Long-Term Cardiovascular Outcomes in Survivors of Breast Cancer: A UK Biobank Study.Journal of the American Heart Association · 2025Article
- ICAM-1-suPAR-CD11b Axis Is a Novel Therapeutic Target for Metastatic Triple-Negative Breast Cancer.Cancers · 2023Article
- Human antibody VFrontiers in oncology · 2023Article
- Urokinase-type plasminogen activator receptor (uPAR) as a therapeutic target in cancer.Journal of translational medicine · 2022Review
- Engineered Cell-Derived Vesicles Displaying Targeting Peptide and Functionalized with Nanocarriers for Therapeutic microRNA Delivery to Triple-Negative Breast Cancer in Mice.Advanced healthcare materials · 2022Article
- Modulation of Cellular Function by the Urokinase Receptor Signalling: A Mechanistic View.Frontiers in cell and developmental biology · 2022Review
- uPAR: An Essential Factor for Tumor Development.Journal of Cancer · 2021Review
- Article
- Improved therapeutic efficacy of quercetin-loaded polymeric nanoparticles on triple-negative breast cancer by inhibiting uPA.RSC advances · 2020Article
- Article
- High baseline soluble urokinase plasminogen activator receptor (suPAR) serum levels indicate adverse outcome after resection of pancreatic adenocarcinoma.Carcinogenesis · 2019Article
- The overexpression of uPA promotes the proliferation and fibrinolytic activity of human umbilical vein endothelial cells.International journal of clinical and experimental pathology · 2019Article
- Transgenic overexpression of humanOncology letters · 2019Article
- Dual-targeting Wnt and uPA receptors using peptide conjugated ultra-small nanoparticle drug carriers inhibited cancer stem-cell phenotype in chemo-resistant breast cancer.Biomaterials · 2018Article
- MicroRNA-645 targets urokinase plasminogen activator and decreases the invasive growth of MDA-MB-231 triple-negative breast cancer cells.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDue to lack of a targeted therapy for the triple-negative breast cancer (TNBC) patients, it is important to explore this aggressive breast cancer type in more detail and to establish novel therapeutic approaches. TNBC is defined negative for the protein expression of oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). One prominent feature of this cancer type is the frequent overexpression of major components of the urokinase-type plasminogen activator system (uPAS) including uPA, its receptor uPAR and the inhibitor PAI-1, which may be valuable as therapeutic targets.
methodsDirect interactions of uPAR with interactors were demonstrated by immunoprecipitations and proximity ligation assays. For stable knockdowns of target proteins, lentiviral vectors were used and the effects were analysed by immunoblottings and using in vitro cell viability, migration and invasion assays. Immunohistochemical and statistical analyses of biomarkers and clinical parameters were conducted in a TNBC cohort (n = 174).
resultsDirect tumour-promoting interactions of uPAR with uPA and the insulin-like growth factor receptor 1 (IGF1R) were shown in TNBC cells and these interactions were significantly reduced (p = 0.001) when uPAR was downregulated. The combined knockdown of uPAR and uPA or IGF1R additively and significantly reduced cell viability, migration and invasion of the model cell lines. In TNBC tissue, the complexes formed by uPAR with uPA or with IGF1R significantly correlated with the histological grade (p = 0.0019) as well as with cathepsin B and D (p ≤ 0.0001) that are implicated in cell invasion and metastasis.
conclusionsOur outcomes show that not only overexpressed biomarkers promote tumourigenesis, but rather their interactions further potentiate tumour progression. This study emphasises the potential of combined approaches targeting uPAR and its interactors with regard to an improved therapy of TNBC.
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