Enteric neural-tumor interactions in gastrointestinal malignancies and therapeutic implications

Figure 1 Tumor-driven remodeling of the enteric neuroglial niche in gastrointestinal cancer: This schematic summarizes three representative routes by which gastrointestinal tumors reshape the enteric neuroglial niche. In gastric mucosa, cholinergic and tuft cell signals amplify neurotrophic support and neural expansion. In colorectal cancer, inflammatory crosstalk between infiltrating monocytes and enteric glia establishes a reciprocal myeloid-promoting circuit. Tumor epithelium can also reprogram enteric glia into a prostaglandin-producing state that reinforces stem-like tumor behavior. Together, these interactions depict the enteric neuroglial network as a dynamic stromal compartment that is actively co-opted to support tumor initiation, progression, and local microenvironmental adaptation. NGF: Nerve growth factor; IL-1: Interleukin 1; IL-6: Interleukin 6; PGE2: Prostaglandin E2; DCLK1: Doublecortin-like kinase 1; SPP1: Secreted phosphoprotein 1; TAM: Tumor-associated macrophage.