ArticleCancer science2026
L1CAM Promotes the Infiltrative Properties of Patient-Derived Glioblastoma Cells.
Article in Cancer science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Mechanical polarity links adhesion-regulated protrusions to directional stability in glioblastoma cell migration.PLoS computational biology · 2026Article
- An L1CAM-Positive Fibroblast-Associated Stromal State Is Associated with Reduced T/NK Cytotoxicity Features in Colorectal Cancer.Biomedicines · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
L1CAM is a member of the immunoglobulin superfamily involved in cell adhesion, migration, and neural development. While several studies have shown an association between L1CAM and glioblastoma (GBM) cell motility, its mechanobiological function in patient-derived primary cultured GBM cells remains insufficiently understood. This study focuses on L1CAM-dependent motility mechanisms in patient-derived GBM cells at the single-cell level. Patient-derived GBM cells were established from GBM tissues using the neurosphere method. L1CAM expression was evaluated by qPCR, western blotting, flow cytometry, and immunocytochemistry. Cell motility was assessed by single-cell tracking. Functional assays included forced expression and antibody-mediated inhibition of L1CAM. Adhesion-clutch behavior and retrograde F-actin flow were analyzed. For in vivo assessment, doxycycline-inducible L1CAM-overexpressing GBM cells were transplanted into mouse brains. L1CAM-high GBM cells showed increased motility on laminin compared to L1CAM-low cells. Anti-L1CAM antibody suppressed migration of L1CAM-high GBM cells, whereas ectopic expression enhanced migration in L1CAM-low GBM cells. L1CAM-positive GBM cells preferentially migrated on laminin rather than fibronectin, while L1CAM-low cells showed no such difference, indicating L1CAM-dependent haptotaxis. Forced L1CAM expression reduced retrograde actin flow velocity and promoted adhesion-clutch formation. In vivo, GBM cells with L1CAM overexpression displayed greater infiltrative capacity 12 weeks posttransplantation. L1CAM expression on GBM cells' surface regulates cell motility through adhesion-clutch mechanisms and substrate sensing. These mechanobiological features suggest that targeting L1CAM may serve as a promising strategy to suppress GBM cells infiltration and improve GBM treatment outcomes.
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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 Socratic graph.