ArticleClinical and translational medicine2026
Neuro-associated SEMA3C
Article in Clinical and translational medicine, 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
backgroundRecent studies have established that the nervous system is not merely a bystander in tumour progression but can actively remodel the tumour microenvironment through the neuro-tumour axis, thereby promoting tumour invasion, metastasis and survival. Semaphorin 3C (SEMA3C) has been reported to regulate tumour migration, angiogenesis and immune suppression, highlighting its potential role in tumour progression. Although the neuro-tumour axis has been identified in multiple cancer types, its role and underlying mechanisms in gastric cancer peritoneal metastasis (GCPM) remain unclear.
methodsWe performed single-nucleus RNA sequencing (snRNA-seq) of GCPM tissues to profile tumour cell heterogeneity and identify tumour cell populations associated with neural-related signalling. Candidate tumour-microenvironmental interactions were further investigated using patient-derived organoids and co-culture models, and the identified signalling axis was validated using corresponding in vivo models.
resultsSnRNA-seq identified a distinct subpopulation of poorly differentiated tumour cells with pronounced stem-like properties and high SEMA3C expression. This subpopulation was associated with neural-related features and interacted with tumour-associated endothelial cells, thereby contributing to remodelling of the metastatic microenvironment. Furthermore, these cells enhanced tumour-endothelial communication by activating the fibroblast growth factor receptor-associated signalling pathway. The transcription factor early B-cell factor 2 (EBF2) regulates the expression of FGF7 within this subpopulation, thereby strengthening FGF7-FGFR2 signalling and promoting tumour progression. Functional validation further demonstrated that SEMA3C depletion impaired organoid growth and tumour-endothelial interactions, whereas disruption of the SEMA3C-EBF2-FGF7-FGFR2 signalling axis attenuated tumour growth and peritoneal tumour burden in vivo. Additional experimental validation supported the potential involvement of neural-related signalling in the SEMA3C-associated tumour cell state.
conclusionsOur findings identify a SEMA3C
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