{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSOX17 is a master transcription factor that orchestrates early cell‐fate decisions in human development. It is essential for the specification of primordial germ cell‐like cells from pluripotent stem cells and for directing endodermal differentiation, thereby marking both extraembryonic and definitive endoderm progenitors. In addition, SOX17 participates in the programming of hemogenic endothelium and arterial identity—processes that underpin hematopoietic stem cell emergence—as well as in neural development, including oligodendrocyte differentiation and the molecular delineation of germ cell tumor subtypes in the testis. These developmental roles are further highlighted by studies showing that a switch from SOX2 to SOX17 occupancy on key promoters pre‐patterns the epigenome to promote endoderm induction and by evidence that SOX17 controls progenitor identity in intermediate states generated during fibroblast dedifferentiation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn multiple cancer types, SOX17 functions predominantly as a tumor suppressor by antagonizing canonical Wnt/β‐catenin signaling. Aberrant DNA hypermethylation of the SOX17 promoter leads to its silencing, which in turn is associated with enhanced cellular proliferation, cell‐cycle deregulation, and increased invasive and metastatic potential in colorectal, hepatocellular, esophageal, lung, gastric, and breast cancers. Disruption of SOX17 function—whether by epigenetic modification or through dysregulation by microRNAs—contributes to aberrant activation of oncogenic pathways and loss of proper differentiation. Consequently, assessment of SOX17 methylation in tumor tissues, circulating tumor cells, or cell‐free DNA has emerged as a promising biomarker for early detection, disease stratification, and prognostication across various malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSOX17 also plays a pivotal role in vascular biology and endothelial cell function. Genetic variants in SOX17 have been linked to pulmonary arterial hypertension and intracranial aneurysm susceptibility. In tumor endothelial cells, its expression modulates angiogenic behavior—where overexpression enhances abnormal vascular sprouting and deletion restores vessel normalization to improve drug delivery. Moreover, SOX17 is upregulated in response to inflammatory injury, promoting endothelial regeneration through activation of proliferation regulators, and its interplay with other transcription factors (such as PAX8) further modulates the secretion of angiogenic factors in ovarian cancer. These multifaceted contributions underscore the importance of SOX17 in maintaining vascular homeostasis in both physiological and pathological contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Cheryle A Séguin, Jonathan S Draper, Andras Nagy, et al. 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