ArticleCancer cell international2009
Stimulation of glioma cell motility by expression, proteolysis, and release of the L1 neural cell recognition molecule.
Article in Cancer cell international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- L1 Cell Adhesion Molecule in Cancer, a Systematic Review on Domain-Specific Functions.International journal of molecular sciences · 2019Pooled it
- L1CAM Promotes the Infiltrative Properties of Patient-Derived Glioblastoma Cells.Cancer science · 2026Article
- Mesenchymal Properties of Glioma Cell Lines.Bulletin of experimental biology and medicine · 2024Article
- Functional Relationships between L1CAM, LC3, ATG12, and Aβ.International journal of molecular sciences · 2024Article
- Knocking out alpha-synuclein in melanoma cells downregulates L1CAM and decreases motility.Scientific reports · 2023Article
- L1CAM-associated extracellular vesicles: A systematic review of nomenclature, sources, separation, and characterization.Journal of extracellular biology · 2022Article
- Exosomal L1CAM Stimulates Glioblastoma Cell Motility, Proliferation, and Invasiveness.International journal of molecular sciences · 2019Article
- Increased L1CAM (CD171) levels are associated with glioblastoma and metastatic brain tumors.Medicine · 2018Article
- A simple and accurate rule-based modeling framework for simulation of autocrine/paracrine stimulation of glioblastoma cell motility and proliferation by L1CAM in 2-D culture.BMC systems biology · 2017Article
- Small-molecule inhibitors of FGFR, integrins and FAK selectively decrease L1CAM-stimulated glioblastoma cell motility and proliferation.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- Extracellular vesicles shed by glioma cells: pathogenic role and clinical value.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- L1CAM stimulates glioma cell motility and proliferation through the fibroblast growth factor receptor.Clinical & experimental metastasis · 2013Article
- Influence of L1-CAM expression of breast cancer cells on adhesion to endothelial cells.Journal of cancer research and clinical oncology · 2013Article
- Comparison of L1 expression and secretion in glioblastoma and neuroblastoma cells.Oncology letters · 2012Article
- L1 stimulation of human glioma cell motility correlates with FAK activation.Journal of neuro-oncology · 2011Article
- Soluble L1CAM promotes breast cancer cell adhesion and migration in vitro, but not invasion.Cancer cell international · 2010Article
- "CRASH"ing with the worm: insights into L1CAM functions and mechanisms.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
- L1CAM: a major driver for tumor cell invasion and motility.Cell adhesion & migrationReview
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMalignant glioma cells are particularly motile and can travel diffusely through the brain parenchyma, apparently without following anatomical structures to guide their migration. The neural adhesion/recognition protein L1 (L1CAM; CD171) has been implicated in contributing to stimulation of motility and metastasis of several non-neural cancer types. We explored the expression and function of L1 protein as a stimulator of glioma cell motility using human high-grade glioma surgical specimens and established rat and human glioma cell lines.
resultsL1 protein expression was found in 17 out of 18 human high-grade glioma surgical specimens by western blotting. L1 mRNA was found to be present in human U-87/LacZ and rat C6 and 9L glioma cell lines. The glioma cell lines were negative for surface full length L1 by flow cytometry and high resolution immunocytochemistry of live cells. However, fixed and permeablized cells exhibited positive staining as numerous intracellular puncta. Western blots of cell line extracts revealed L1 proteolysis into a large soluble ectodomain (~180 kDa) and a smaller transmembrane proteolytic fragment (~32 kDa). Exosomal vesicles released by the glioma cell lines were purified and contained both full-length L1 and the proteolyzed transmembrane fragment. Glioma cell lines expressed L1-binding alphavbeta5 integrin cell surface receptors. Quantitative time-lapse analyses showed that motility was reduced significantly in glioma cell lines by 1) infection with an antisense-L1 retroviral vector and 2) L1 ectodomain-binding antibodies.
conclusionOur novel results support a model of autocrine/paracrine stimulation of cell motility in glioma cells by a cleaved L1 ectodomain and/or released exosomal vesicles containing L1. This mechanism could explain the diffuse migratory behavior of high-grade glioma cancer cells within the brain.
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Registered trials
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