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Peer-reviewedCC BY 4.0Frontiers in Neurology

Functional divergence of the synapsin family in glioblastoma: Synapsin III as a candidate differentiation-restoring node

  • Xiangyu Dai1
  • Yujie Ji1
  • Zheng Cai1
  • Haixin Zeng1
  • Yi Li1
  • Haining Zhou1
  • Xu Zhang2
  • Bing Li1
  1. 1Department of Neurosurgery, Jiangnan University Medical Center, Wuxi No.2 People's Hospital, Jiangnan University, Wuxi, China
  2. 2Clinical Medical Research Center, Jiangnan University Medical Center, Wuxi No.2 People's Hospital, Jiangnan University, Wuxi, China
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Abstract

Glioblastoma (GBM) remains an aggressive adult primary brain tumor despite surgery, radiotherapy and temozolomide-based chemotherapy, partly because glioblastoma stem cells (GSCs) retain self-renewal capacity, lineage plasticity and therapeutic resistance. Cancer neuroscience has shown that glioma cells receive activity-dependent neuronal signals and exploit neural circuits to support tumor growth and invasion. Synaptic proteins may therefore regulate both neuron-glioma communication and tumor-cell state. Synapsin I, II, and III share conserved N-terminal domains but differ in C-terminal architecture, developmental expression and physiological function. An emerging model of functional divergence in GBM is supported by a recent preclinical study comparing Synapsin III with Synapsin I and II. In the tested GSC models, increasing Synapsin III promoted a neuronal-like differentiated phenotype through a neuregulin 3 (NRG3)-JAG1-NOTCH1 mechanism, with reduced stemness and proliferative growth. This review integrates structural, physiological and GBM-focused evidence to examine how the developmental functions of Synapsin III may be repurposed in malignant stem-like cells. Independent replication, durable loss of tumorigenicity and tumor-selective delivery are priorities for translation. Synapsin III is a candidate differentiation-restoring node whose clinical relevance remains to be established.

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Cite

BibTeXRIS
BibTeX
@article{dai2026functional,
  title = {{Functional divergence of the synapsin family in glioblastoma: Synapsin III as a candidate differentiation-restoring node}},
  author = {Xiangyu Dai and Yujie Ji and Zheng Cai and Haixin Zeng and Yi Li and Haining Zhou and Xu Zhang and Bing Li},
  journal = {Frontiers in Neurology},
  year = {2026},
  month = oct,
  doi = {10.3389/fneur.2026.1976698},
  url = {https://doi.org/10.3389/fneur.2026.1976698},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Functional divergence of the synapsin family in glioblastoma: Synapsin III as a candidate differentiation-restoring node
AU  - Xiangyu Dai
AU  - Yujie Ji
AU  - Zheng Cai
AU  - Haixin Zeng
AU  - Yi Li
AU  - Haining Zhou
AU  - Xu Zhang
AU  - Bing Li
PY  - 2026
DA  - 2026/10/12
JO  - Frontiers in Neurology
DO  - 10.3389/fneur.2026.1976698
UR  - https://doi.org/10.3389/fneur.2026.1976698
AB  - Glioblastoma (GBM) remains an aggressive adult primary brain tumor despite surgery, radiotherapy and temozolomide-based chemotherapy, partly because glioblastoma stem cells (GSCs) retain self-renewal capacity, lineage plasticity and therapeutic resistance. Cancer neuroscience has shown that glioma cells receive activity-dependent neuronal signals and exploit neural circuits to support tumor growth and invasion. Synaptic proteins may therefore regulate both neuron-glioma communication and tumor-cell state. Synapsin I, II, and III share conserved N-terminal domains but differ in C-terminal architecture, developmental expression and physiological function. An emerging model of functional divergence in GBM is supported by a recent preclinical study comparing Synapsin III with Synapsin I and II. In the tested GSC models, increasing Synapsin III promoted a neuronal-like differentiated phenotype through a neuregulin 3 (NRG3)-JAG1-NOTCH1 mechanism, with reduced stemness and proliferative growth. This review integrates structural, physiological and GBM-focused evidence to examine how the developmental functions of Synapsin III may be repurposed in malignant stem-like cells. Independent replication, durable loss of tumorigenicity and tumor-selective delivery are priorities for translation. Synapsin III is a candidate differentiation-restoring node whose clinical relevance remains to be established.
SN  - 1664-2295
ER  -