ReviewTranslational cancer research2026
Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.
Review in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
High-grade gliomas (HGGs), particularly isocitrate dehydrogenase (IDH)-wild-type glioblastoma (GBM), remain highly lethal despite increasingly complex, tumor-intrinsic therapies. Converging evidence from models and human studies now positions neuronal activity as a core driver of glioma growth, invasion and epileptogenesis. This review synthesizes data on a mechanistically defined neuro-glioma circuit that links activity-dependent neuroligin-3 (NLGN3) shedding by the sheddase a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) ADAM10 with the formation and strengthening of neuron-glioma α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor synapses. Neuronal and oligodendroglial firing activates ADAM10, generating soluble NLGN3 (sNLGN3) that reprograms glioma cells toward a highly neural, synapse-competent state through kinase, epigenetic and mechanosensory pathways, including LYN proto-oncogene, Src family tyrosine kinase (LYN), phosphoinositide 3-kinase (PI3K)-mechanistic target of rapamycin (mTOR) and chondroitin sulfate proteoglycan 4 (CSPG4)-Piezo-type mechanosensitive ion channel component 1 (PIEZO1) signaling. Reprogrammed tumor cells then assemble calcium-permeable AMPA receptors and bona fide neuron-glioma synapses, receive excitatory input and propagate calcium waves across tumor networks, which in turn amplify peritumoral hyperexcitability and seizures, closing a positive feedback loop of activity-dependent growth. On this basis, we outline an "actionable circuit" spanning neuronal activity, NLGN3-ADAM10 shedding, intracellular signaling, synaptic integration and network remodeling, and we organize emerging pharmacologic and device-based strategies into a circuit-breaking framework that includes activity dampening, inhibition of NLGN3 shedding, blockade of downstream signaling and AMPA synapses, and network-level modulation. Finally, we highlight key translational challenges and opportunities in target selectivity, brain delivery, biomarker development and adaptive trial design, arguing that multidimensional, circuit-informed interventions may complement standard surgery, radiochemotherapy and molecular targeting in selected patients with activity-driven glioma.
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