ArticleMolecular cancer research : MCR2008
Sphingosine-1-phosphate and interleukin-1 independently regulate plasminogen activator inhibitor-1 and urokinase-type plasminogen activator receptor expression in glioblastoma cells: implications for invasiveness.
Article in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Sphingosine 1-phosphate (S1P) signaling in glioblastoma multiforme-A systematic review.International journal of molecular sciences · 2017Pooled it
- The physiological and pathological effects of sphingolipid metabolism and signaling in the central nervous system.Brain pathology (Zurich, Switzerland) · 2026Review
- Sphingolipid Signaling and Complement Activation in Glioblastoma: A Promising Avenue for Therapeutic Intervention.BioChem · 2024Article
- The evaluation of six genes combined value in glioma diagnosis and prognosis.Journal of cancer research and clinical oncology · 2023Article
- Article
- Sphingosine-1-Phosphate in the Tumor Microenvironment: A Signaling Hub Regulating Cancer Hallmarks.Cells · 2020Review
- Review
- Bioactive lysolipids in cancer and angiogenesis.Pharmacology & therapeutics · 2019Review
- Review
- Sphingosine 1-Phosphate and Atherosclerosis.Journal of atherosclerosis and thrombosis · 2018Review
- Vehicle-dependent Effects of Sphingosine 1-phosphate on Plasminogen Activator Inhibitor-1 Expression.Journal of atherosclerosis and thrombosis · 2017Article
- DES-TOMATO: A Knowledge Exploration System Focused On Tomato Species.Scientific reports · 2017Article
- The emerging role of FTY720 (Fingolimod) in cancer treatment.Oncotarget · 2016Review
- Sphingosine 1-phosphate is a ligand for peroxisome proliferator-activated receptor-γ that regulates neoangiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Interference with distinct steps of sphingolipid synthesis and signaling attenuates proliferation of U87MG glioma cells.Biochemical pharmacology · 2015Article
- Leptin induces upregulation of sphingosine kinase 1 in oestrogen receptor-negative breast cancer via Src family kinase-mediated, janus kinase 2-independent pathway.Breast cancer research : BCR · 2014Article
- Export of sphingosine-1-phosphate and cancer progression.Journal of lipid research · 2014Review
- Induction of chemokine (C-C motif) ligand 2 by sphingosine-1-phosphate signaling in neuroblastoma.Journal of pediatric surgery · 2014Article
- Interleukin-1-induced changes in the glioblastoma secretome suggest its role in tumor progression.Journal of proteomics · 2014Article
- Protein kinase D2 regulates migration and invasion of U87MG glioblastoma cells in vitro.Experimental cell research · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Glioblastoma multiforme is an invasive primary brain tumor, which evades the current standard treatments. The invasion of glioblastoma cells into healthy brain tissue partly depends on the proteolytic and nonproteolytic activities of the plasminogen activator system proteins, including the urokinase-type plasminogen activator (uPA), plasminogen activator inhibitor 1 (PAI-1), and a receptor for uPA (uPAR). Here we show that sphingosine-1-phosphate (S1P) and the inflammatory mediator interleukin-1 (IL-1) increase the mRNA and protein expression of PAI-1 and uPAR and enhance the invasion of U373 glioblastoma cells. Although IL-1 enhanced the expression of sphingosine kinase 1 (SphK1), the enzyme that produces S1P, down-regulation of SphK1 had no effect on the IL-1-induced uPAR or PAI-1 mRNA expression, suggesting that these actions of IL-1 are independent of S1P production. Indeed, the S1P-induced mRNA expression of uPAR and PAI-1 was blocked by the S1P(2) receptor antagonist JTE013 and by the down-regulation of S1P(2) using siRNA. Accordingly, the inhibition of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 and Rho-kinase, two downstream signaling cascades activated by S1P(2), blocked the activation of PAI-1 and uPAR mRNA expression by S1P. More importantly, the attachment of glioblastoma cells was inhibited by the addition of exogenous PAI-1 or siRNA to uPAR, whereas the invasion of glioblastoma cells induced by S1P or IL-1 correlated with their ability to enhance the expression of PAI-1 and uPAR. Collectively, these results indicate that S1P and IL-1 activate distinct pathways leading to the mRNA and protein expression of PAI-1 and uPAR, which are important for glioblastoma invasiveness.
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