{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTenascin‑C is a multifunctional matricellular glycoprotein that is dynamically expressed in pathological settings. It is rapidly induced by proinflammatory cytokines (for example, via TGF‑β/Smad, Sp1, and Ets1 signaling cascades) and deposited at sites of tissue injury, chronic inflammation, and abnormal extracellular matrix (ECM) remodeling. Acting as an endogenous danger signal, Tenascin‑C engages Toll‑like receptor 4 (TLR4) to promote robust cytokine production and sustain persistent inflammation in disorders such as rheumatoid arthritis and systemic sclerosis. Moreover, its deposition is finely regulated by ECM partners like periostin, which organize its integration within the matrix, thereby modulating adhesion and cell–matrix interactions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, Tenascin‑C plays a prominent role in promoting tumor progression, invasion, and metastasis. It is secreted by stromal cells such as myofibroblasts to induce an epithelial–mesenchymal transition (EMT)–like change and to modulate integrin‐mediated signaling that alters cytoskeletal organization. This contributes to enhanced migratory and invasive capacities in a variety of malignancies including colon cancer, breast cancer, gliomas, lung adenocarcinoma, prostate cancer, and osteosarcoma. In glioblastoma, for example, Notch2‐dependent transactivation of Tenascin‑C correlates with aggressive perivascular invasion, while in breast tumors, alternatively spliced variants localize to invasive fronts and herald a poorer prognosis. Furthermore, Tenascin‑C can also impair local T cell responses in the tumor microenvironment through integrin interactions, thus facilitating immune evasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in inflammation and tumorigenesis, Tenascin‑C is a critical regulator of tissue remodeling and repair. It modulates cell adhesion and matrix contraction during wound healing and influences angiogenic responses by binding a diverse array of growth factors through its fibronectin type III domains. In the cardiovascular system, its re‑expression after myocardial injury contributes to both reparative and fibrotic processes. Additionally, Tenascin‑C participates in the regulation of skeletal muscle responses following eccentric exercise and even exerts antiviral activity, as demonstrated by its ability to neutralize HIV‑1 in breast milk. Together, these findings underscore Tenascin‑C’s versatile functions in orchestrating cellular responses to mechanical, inflammatory, and infectious challenges, as well as its potential as a prognostic biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kim Midwood, Sandra Sacre, Anna M Piccinini, et al. 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