{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSOX18 is a critical transcription factor that orchestrates aspects of embryonic development, most notably in the formation and differentiation of hair follicles, blood vessels, and lymphatic vessels. Mutations in SOX18 can lead to syndromes such as hypotrichosis‐lymphedema–telangiectasia—with some cases also manifesting cardiovascular and renal defects—thereby underscoring its essential role in vascular development and integrity. These observations, derived from genetic studies of both recessive and dominant SOX18 mutations, highlight its indispensable function in normal endothelial cell fate and tissue homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the vascular endothelium, SOX18 plays a central role in establishing and maintaining the barrier function by directly regulating genes encoding tight junction proteins—such as claudin‐5—and by modulating endothelial cell–cell adhesion. Inflammatory stimuli, via NF‐κB signaling, can repress SOX18 transcription thereby compromising barrier integrity, while its unique capacity to dimerize refines the specificity of endothelial gene regulation and vascular patterning. These mechanistic insights, uncovered in both in vitro and in vivo models, emphasize that a precise balance of SOX18 activity is essential for proper endothelial function."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_fs", "start_ref": "10", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its developmental roles, dysregulated SOX18 expression has emerged as a key driver in a wide spectrum of human cancers. In tumors ranging from breast, pancreatic, non‐small cell lung, gastric, cervical, and hepatocellular carcinomas to prostate, laryngeal, papillary thyroid, bladder, Kaposi sarcoma, and osteosarcoma, elevated SOX18 levels correlate with enhanced proliferation, epithelial‐to‐mesenchymal transition, invasion, and metastasis. Mechanistically, SOX18 exerts its oncogenic effects by modulating the expression of downstream effectors—including cyclin D1, c‐Myc, matrix metalloproteinases, PDGFB, IGF1R, and other factors—and interfacing with critical signaling cascades such as gp130/JAK2/STAT3, Wnt/β‐catenin, and Hedgehog. Its expression is further fine‐tuned by microRNAs as well as by transcriptional regulators (e.g., Sp3, ZBP‑89, and NF‑Y), and dominant‑negative mutations in SOX18 can disrupt not only its normal activity but also that of its interacting partners. Collectively, these studies reveal that aberrant SOX18 activity contributes to tumor progression and may serve as both a prognostic marker and a promising therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "19"}, {"type": "fg_f", "ref": "11"}, {"type": "fg_fs", "start_ref": "20", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Alexandre Irrthum, Koenraad Devriendt, David Chitayat, et al. 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