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Related Experiment Video

Updated: Jun 2, 2026

Co-culture of Glutamatergic Neurons and Pediatric High-Grade Glioma Cells Into Microfluidic Devices to Assess Electrical Interactions
07:39

Co-culture of Glutamatergic Neurons and Pediatric High-Grade Glioma Cells Into Microfluidic Devices to Assess Electrical Interactions

Published on: November 17, 2021

C1QL1: A Long-range Signal Orchestrating Glioma Connectivity and Synaptic Remodeling.

Yujia Li1, Jeremy C Borniger1

  • 1Cancer Center and Neuroscience Division, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York.

Cancer Discovery
|June 1, 2026
PubMed
Summary
This summary is machine-generated.

Glioblastoma cells release C1QL1, activating RAC1 to fuel tumor growth and synapse changes. Inhibiting RAC1 may prevent glioblastoma (GBM) recurrence by blocking these harmful processes.

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Last Updated: Jun 2, 2026

Co-culture of Glutamatergic Neurons and Pediatric High-Grade Glioma Cells Into Microfluidic Devices to Assess Electrical Interactions
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Co-culture of Glioblastoma Stem-like Cells on Patterned Neurons to Study Migration and Cellular Interactions
10:08

Co-culture of Glioblastoma Stem-like Cells on Patterned Neurons to Study Migration and Cellular Interactions

Published on: February 24, 2021

Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Cellular signaling

Background:

  • Glioblastoma (GBM) is an aggressive brain tumor.
  • Tumor cells interact with the surrounding neural microenvironment.
  • Synaptic plasticity and remodeling are crucial in neural networks.

Purpose of the Study:

  • To investigate the role of C1QL1 secreted by GBM cells.
  • To identify the molecular mechanisms underlying GBM-neuron interactions.
  • To explore potential therapeutic targets for GBM.

Main Methods:

  • Analysis of C1QL1 secretion by GBM cells.
  • Investigating the binding of C1QL1 to BAI3 receptors.
  • Assessing RAC1 activation in tumor and neuronal cells.
  • Evaluating the effects of RAC1 inhibition on tumor growth and synapses.

Main Results:

  • GBM cells secrete C1QL1, which binds to BAI3 on tumor and neuronal cells.
  • This interaction activates RAC1, promoting tumor microtube formation.
  • Malignant synapse formation and remodeling of normal synapses are observed.
  • Targeted inhibition of RAC1 disrupts these processes.

Conclusions:

  • C1QL1-BAI3-RAC1 signaling is a key pathway in GBM progression.
  • Blocking RAC1 offers a potential strategy to prevent GBM recurrence.
  • Targeting cell-cell communication presents a novel therapeutic avenue for brain tumors.