{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPeriostin (POSTN) is a multifunctional matricellular protein that promotes tumor progression and metastasis by orchestrating numerous events in the tumor microenvironment. In a variety of human cancers—including glioblastoma, colon, ovarian, breast, head and neck, esophageal, and non‐small‐cell lung carcinomas—POSTN is frequently overexpressed and secreted by either cancer cells or cancer‐associated stromal fibroblasts. Its actions include the recruitment of tumor‐promoting macrophages, the facilitation of epithelial–mesenchymal transition, and enhancement of cell survival, invasion and angiogenesis via integrin‐mediated activation of downstream signaling cascades such as focal adhesion kinase (FAK), PI3K/Akt, and Src. These findings underscore POSTN’s pivotal role in modulating adhesion, migration, and survival in malignant cells, thereby fostering metastasis and aggressive disease behavior."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn non‐neoplastic contexts, POSTN plays a central role in orchestrating tissue repair, remodeling and fibrogenesis. In the injured heart, for instance, POSTN is up‐regulated in the infarct border and promotes the recruitment and differentiation of activated fibroblasts, thereby facilitating collagen fibrillogenesis and stabilization of the myocardial extracellular matrix. Similarly, in the lung and skin, POSTN contributes to wound healing and chronic remodeling by modulating epithelial–mesenchymal cross‐talk, enhancing fibroblast activation and extracellular matrix stiffness, and even regulating eosinophil adhesion in allergic conditions. Moreover, studies in bone and vascular smooth muscle cells demonstrate that POSTN regulates matrix mineralization and cell motility via integrin/FAK signalling, while its induction in renal and fibrotic disorders further implicates it as a mediator of pathologic extracellular matrix adaptation in response to mechanical and cytokine‐driven stress."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies reveal that POSTN serves as an integrative mediator linking cytokine and growth factor signals (such as TGF‐β, IL‐4 and IL‐13) to changes in extracellular matrix composition, cell adhesion and motility across both cancerous and fibrotic settings. By modulating key intracellular effectors—including FAK, Src and Akt—POSTN not only supports tumor–stromal interactions and metastatic niche formation but also drives maladaptive tissue remodeling in chronic inflammatory and fibrotic diseases. This cross‐cutting role positions POSTN as an attractive biomarker for disease progression and an appealing target for therapeutic intervention in a wide spectrum of clinical conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "38", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lindsay Gillan, Daniela Matei, David A Fishman, et al. 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