ArticleOncotarget2014
Melanoma cell therapy: Endothelial progenitor cells as shuttle of the MMP12 uPAR-degrading enzyme.
Article in Oncotarget, 2014. 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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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Targeting the microbiota-miRNA-protease axis: A new therapeutic avenue in melanoma.The FEBS journal · 2026Review
- Unveiling the Role of Tryptophan 2,3-Dioxygenase in the Angiogenic Process.Pharmaceuticals (Basel, Switzerland) · 2024Article
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- The Transcriptional Landscape ofInternational journal of molecular sciences · 2022Article
- Enhanced Vasculogenic Capacity Induced by 5-Fluorouracil Chemoresistance in a Gastric Cancer Cell Line.International journal of molecular sciences · 2021Article
- Enhanced Antitumoral Activity and Photoacoustic Imaging Properties of AuNP-Enriched Endothelial Colony Forming Cells on Melanoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- uPAR: An Essential Factor for Tumor Development.Journal of Cancer · 2021Review
- CRISPR/Cas9 uPAR Gene Knockout Results in Tumor Growth Inhibition, EGFR Downregulation and Induction of Stemness Markers in Melanoma and Colon Carcinoma Cell Lines.Frontiers in oncology · 2021Article
- Cell-Mediated Release of Nanoparticles as a Preferential Option for Future Treatment of Melanoma.Cancers · 2020Review
- microRNA-378a-5p iS a novel positive regulator of melanoma progression.Oncogenesis · 2020Article
- Article
- Gene Therapy with Cytosine Deaminase and Endostatin Fusion Gene Mediated by Endothelial Progenitor Cells in Hepatomas.Cancer management and research · 2020Article
- MMP-12, Secreted by Pro-Inflammatory Macrophages, Targets Endoglin in Human Macrophages and Endothelial Cells.International journal of molecular sciences · 2019Article
- CRISPR/Cas9 nickase mediated targeting of urokinase receptor gene inhibits neuroblastoma cell proliferation.Oncotarget · 2018Article
- Pro-apoptotic effect of TRAIL-transfected endothelial progenitor cells on glioma cells.Oncology letters · 2018Article
- Tissue regeneration using endothelial colony-forming cells: promising cells for vascular repair.Pediatric research · 2018Review
- Delivery systems of CRISPR/Cas9-based cancer gene therapy.Journal of biological engineering · 2018Review
- Article
- Matrix metalloproteinase-12 expression is increased in cutaneous melanoma and associated with tumor aggressiveness.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Inhibition of uPAR-TGFβ crosstalk blocks MSC-dependent EMT in melanoma cells.Journal of molecular medicine (Berlin, Germany) · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor for the urokinase-type plasminogen activator (uPAR) accounts for many features of cancer progression, and is therefore considered a target for anti-tumoral therapy. Only full length uPAR mediates tumor progression. Matrix-metallo-proteinase-12 (MMP12)-dependent uPAR cleavage results into the loss of invasion properties and angiogenesis. MMP12 can be employed in the field of "targeted therapies" as a biological drug to be delivered directly in patient's tumor mass. Endothelial Progenitor Cells (EPCs) are selectively recruited within the tumor and could be used as cellular vehicles for delivering anti-cancer molecules. The aim of our study is to inhibit cancer progression by engeneering ECFCs, a subset of EPC, with a lentivirus encoding the anti-tumor uPAR-degrading enzyme MMP12. Ex vivo manipulated ECFCs lost the capacity to perform capillary morphogenesis and acquired the anti-tumor and anti-angiogenetic activity. In vivo MMP12-engineered ECFCs cleaved uPAR within the tumor mass and strongly inhibited tumor growth, tumor angiogenesis and development of lung metastasis. The possibility to exploit tumor homing and activity of autologous MMP12-engineered ECFCs represents a novel way to combat melanoma by a "personalized therapy", without rejection risk. The i.v. injection of radiolabelled MMP12-ECFCs can thus provide a new theranostic approach to control melanoma progression and metastasis.
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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.