{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nUNC5C is a transmembrane receptor for netrin‐1 that functions as a “dependence receptor” during development. When not bound to its ligand, UNC5C actively induces apoptosis, a property that is critical for proper axon guidance and cellular migration. Early studies showed that UNC5C—and its homologs—mediate repulsive cues in the developing nervous system and thus help shape neural connectivity. These findings established UNC5C as a pivotal regulatory element in both neural patterning and in the prevention of inappropriate cell survival."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn parallel, multiple studies have documented that UNC5C acts as a tumor suppressor, with its expression frequently reduced in diverse cancers. Aberrant epigenetic events—such as promoter hypermethylation and chromatin remodeling—as well as loss of heterozygosity and missense mutations, have been observed in colorectal, colon, and other solid tumors. These alterations compromise the pro‐apoptotic function of UNC5C, thereby supporting tumor cell survival and promoting malignant transformation. In addition, the potential use of pharmacogenomic and demethylating approaches underlines the clinical relevance of restoring UNC5C function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurther investigations have expanded the oncogenic landscape in which UNC5C is involved. Studies in renal cell carcinoma, familial colorectal cancer, and even bladder cancer indicate that beyond epigenetic silencing, genetic alterations in UNC5C occur across multiple tumor types. In these contexts, rare germline variants have been evaluated—with evidence suggesting that while some alterations may co‐segregate with disease, their overall impact on hereditary cancer risk is limited. In addition, interactions between UNC5C and other guidance molecules (for example, DSCAM) have been implicated in modulating cell migration and integrin‐dependent signaling, further contributing to its multifaceted role in tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the nervous system and beyond, rare coding mutations in UNC5C have been linked to increased neuronal vulnerability. For instance, the T835M mutation is associated with enhanced sensitivity to neurotoxic insults, contributing to late‐onset Alzheimer’s disease and altered neuroimaging markers of atrophy. Polymorphism studies further suggest that variations in UNC5C may affect hippocampal volume and cognitive resilience. Moreover, through its interactions that regulate axon repulsion and growth cone collapse, UNC5C is implicated in psychiatric disorders, while its dysregulation in non‐neuronal tissues has been related to changes in breast cancer metastasis and even abnormal scarring processes such as keloid formation. Together, these findings underscore the multifaceted roles of UNC5C in cell fate decisions across both neural and non‐neural systems."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Karine Thiebault, Laetitia Mazelin, Laurent Pays, et al. 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