{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTHY1 (also known as CD90) is emerging as a critical molecule in cancer biology, where its cell‐surface expression defines distinct cancer stem cell populations and modulates tumorigenic behavior. In hepatocellular, esophageal, glioblastoma, lung, gastric, ovarian and other malignancies, THY1 marks subpopulations that are endowed with self‐renewal capacity, aggressive growth, metastatic potential and chemoresistance. In some cancer types, THY1 expression is associated with the activation of key signaling pathways – for example, Notch and SHH/Gli as well as downstream IL6/JAK2/STAT3 – which further promote invasion and survival, whereas its loss (often via epigenetic promoter methylation) has been linked to suppressed tumorigenicity and cell cycle arrest. Collectively, these studies indicate that THY1 functions not only as a surrogate marker for cancer stem cells but also as a regulator of tumor initiation and progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn mesenchyme‐derived cells, THY1 expression distinguishes functionally specialized fibroblast and stromal subpopulations that have profound effects on tissue homeostasis and repair. Experimental evidence in primary fibroblasts from human myometrium, orbit, lung and synovial fluid reveals that THY1 expression pre‐determines differentiation trajectories—promoting myofibroblastic, contractile phenotypes and regulating extracellular matrix remodeling—while its absence favors adipogenic or alternative lineage choices. Epigenetic inactivation of the THY1 gene in certain contexts correlates with a fibrogenic and pro‐inflammatory cellular phenotype, underlining its key role in normal tissue integrity as well as in the pathogenesis of fibrotic and stromal disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTHY1 also functions as an important adhesion molecule that mediates cell–cell and cell–matrix interactions. Through direct binding to diverse integrins—including Mac‐1, beta2, and alphavβ3—and co‐receptors such as syndecan‐4, THY1 facilitates firm adhesion, transendothelial migration and dynamic mechanotransduction signals that are critical for inflammatory cell recruitment as well as tumor cell adhesion and metastatic dissemination. Moreover, by modulating mesenchymal stem cell fate, THY1 influences processes as varied as MSC differentiation in adipogenic/osteogenic contexts and vascular niche interactions. These multifaceted adhesive interactions enable THY1 to act as a molecular bridge in both inflammatory and neoplastic microenvironments."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Harindra R Abeysinghe, Qing Cao, Jia Xu, et al. 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