Tumor Microenvironment Interactions in Glioblastoma
Summary
Glioblastoma is characterised by a richly interactive microenvironment that shapes tumour growth, invasion and therapeutic resistance. Within this milieu, cancer cells coexist with stromal, vascular and immune elements embedded in a dynamic extracellular matrix. Glioma-initiating cells form specialised niches sustained by secreted factors, glycoproteins and biophysical cues that promote self-renewal and plasticity. Aberrant angiogenesis supplies nutrients and creates hypoxic zones that further drive invasiveness and immunosuppression. Extracellular matrix remodelling proteins and matricellular glycoproteins such as tenascin C enable migratory pathways and impede immune cell infiltration. Integrin-mediated adhesion to matrix components regulates intracellular signalling cascades, including PI3K/AKT and MAPK, fostering survival and chemoresistance. Moreover, metabolic reprogramming and epigenetic modifications in glioblastoma cells are influenced by oxygen tension and matrix stiffness. Crosstalk between tumour cells and resident microglia or infiltrating macrophages establishes a pro-tumoural inflammatory network, while platelets and fibroblast-like cells contribute further complexity through release of growth factors and proteases. Understanding these interwoven processes has led to emerging strategies targeting matrix-receptor interactions, vascular normalisation and niche disruption, offering the potential to overcome the adaptive resilience of glioblastoma.
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Tumor Microenvironment Interactions in Glioblastoma publication trend
The graph below shows the total number of articles in tumor microenvironment interactions in glioblastoma across all publications each year (not limited to Nature Index journals).
Technical terms
Tumour microenvironment (TME): The complex milieu of non-malignant cells, extracellular matrix and soluble factors surrounding tumour cells.
Glioma-initiating cells (GICs): A subpopulation of self-renewing tumour cells with stem-like properties that drive recurrence.
Extracellular matrix (ECM): A network of proteins and polysaccharides providing structural support and regulatory signals to cells.
Matricellular proteins: Non-structural ECM components that modulate cell-matrix interactions and signalling.
Integrins: Transmembrane receptors that bind ECM ligands and initiate intracellular signalling pathways.
Chondroitin sulfate proteoglycan 4 (CSPG4): A cell surface proteoglycan modified by chondroitin sulfate, implicated in stem-cell niche maintenance.
References
- Chondroitin sulfate modification of CSPG4 regulates the maintenance and differentiation of glioma-initiating cells via integrin-associated signaling. Journal of Biological Chemistry (2024).
- Matricellular protein tenascin C: Implications in glioma progression, gliomagenesis, and treatment. Frontiers in Oncology (2022).
- Tenascin C Promotes Glioma Cell Malignant Behavior and Inhibits Chemosensitivity to Paclitaxel via Activation of the PI3K/AKT Signaling Pathway. Journal of Molecular Neuroscience (2021).
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