ArticleCellular oncology (Dordrecht, Netherlands)2016
Small-molecule inhibitors of FGFR, integrins and FAK selectively decrease L1CAM-stimulated glioblastoma cell motility and proliferation.
Article in Cellular oncology (Dordrecht, Netherlands), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 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
- Article
- A human iPSC-based neural spheroid platform for modelling glioblastoma infiltration using high-content imaging.Scientific reports · 2025Article
- Near-Infrared Photoimmunotherapy in Brain Tumors-An Unexplored Frontier.Pharmaceuticals (Basel, Switzerland) · 2025Review
- QSOX1 Modulates Glioblastoma Cell Proliferation and Migration In Vitro and Invasion In Vivo.Cancers · 2024Article
- Article
- Knocking out alpha-synuclein in melanoma cells downregulates L1CAM and decreases motility.Scientific reports · 2023Article
- Review
- Biobanked Glioblastoma Patient-Derived Organoids as a Precision Medicine Model to Study Inhibition of Invasion.International journal of molecular sciences · 2021Article
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- L1cam curbs the differentiation of adult-born hippocampal neurons.Stem cell research · 2020Article
- Role of exosomes in malignant glioma: microRNAs and proteins in pathogenesis and diagnosis.Cell communication and signaling : CCS · 2020Review
- Sialylation of FGFR1 by ST6Gal‑I overexpression contributes to ovarian cancer cell migration and chemoresistance.Molecular medicine reports · 2020Article
- L1CAM High Expression Associates with Poor Prognosis in Glioma but Does Not Correlate with C11orf95-RELA Fusion.BioMed research international · 2020Article
- Combined proteomics/miRNomics of dendritic cell immunotherapy-treated glioblastoma patients as a screening for survival-associated factors.NPJ vaccines · 2020Article
- Exosomal L1CAM Stimulates Glioblastoma Cell Motility, Proliferation, and Invasiveness.International journal of molecular sciences · 2019Article
- Microarray gene profiling analysis of glioblastoma cell line U87 reveals suppression of theArchives of medical science : AMS · 2019Article
- Establishing cut-off points with clinical relevance for bcl-2, cyclin D1, p16, p21, p27, p53, Sox11 and WT1 expression in glioblastoma - a short report.Cellular oncology (Dordrecht, Netherlands) · 2018Article
- Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2.Bioscience reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe cell adhesion/recognition protein L1CAM (L1; CD171) has previously been shown to act through integrin, focal adhesion kinase (FAK) and fibroblast growth factor receptor (FGFR) signaling pathways to increase the motility and proliferation of glioblastoma cells in an autocrine/paracrine manner. Here, we investigated the effects of clinically relevant small-molecule inhibitors of the integrin, FAK and FGFR signaling pathways on glioblastoma-derived cells to determine their effectiveness and selectivity for diminishing L1-mediated stimulation.
methodsThe effects of the FGFR inhibitor PD173074, the FAK inhibitors PF431396 and Y15 and the αvβ3/αvβ5 integrin inhibitor cilengitide were assessed in L1-positive and L1-negative variants of the human glioblastoma-derived cell lines T98G and U-118 MG. Their motility and proliferation were quantified using time-lapse microscopy and DNA content/cell cycle analyses, respectively.
resultsThe application of all four inhibitors resulted in reductions in L1-mediated motility and proliferation rates of L1-positive glioblastoma-derived cells, down to the level of L1-negative cells when used at nanomolar concentrations, whereas no or much smaller reductions in these rates were obtained in L1-negative cells. In addition, we found that single inhibitor treatment resulted in maximum effects (i.e., combinations of FAK or integrin inhibitors with the FGFR inhibitor were rarely more effective). These results suggest that FAK may act as a point of convergence between the integrin and FGFR signaling pathways stimulated by L1 in these cells.
conclusionsWe here show for the first time that small-molecule inhibitors of FGFR, integrins and FAK effectively and selectively abolish L1-stimulated migration and proliferation of glioblastoma-derived cells. Our results suggest that these inhibitors have the potential to reduce the aggressiveness of high-grade gliomas expressing L1.
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