{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nVersican (VCAN) is a large extracellular matrix proteoglycan that plays key roles in tissue architecture and remodeling. In the vasculature and various developmental contexts, VCAN is prominently upregulated after injury and during remodeling processes. Its modular structure—including globular domains that bind hyaluronan, link protein, and other matrix components—enables formation of expanded, viscoelastic pericellular matrices that regulate smooth muscle cell proliferation, migration, and elastic fiber assembly. Versican accumulation is implicated in vascular diseases such as atherosclerosis, restenosis, and aneurysm formation, as well as in myocardium remodeling following infarction. Moreover, VCAN participates in normal developmental processes including hair follicle morphogenesis and maintenance of valve and ocular integrity, with mutations in the VCAN gene underlying conditions such as Wagner syndrome and abnormalities in benign prostatic hyperplasia."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the cancer context, VCAN is frequently overexpressed and contributes to multiple aspects of tumor progression and metastasis. In several malignancies—including breast, melanoma, glioma, ovarian, hepatocellular, bladder, and renal cancers—upregulated VCAN modulates cell–matrix interactions that affect adhesion, migration, and invasion. Versican supports the epithelial-to-mesenchymal transition (EMT) and, intriguingly, may induce a mesenchymal-to-epithelial transition (MET) in metastatic settings through paracrine secretion from tumor‐associated cells. Its interactions with integrins and cell surface receptors activate survival and signaling pathways (such as EGFR–PI3K–AKT), while its engagement with inflammatory receptors (e.g., TLRs) governs cytokine secretion and immune cell recruitment. Furthermore, post‐transcriptional regulation by microRNAs and transcription factors (including FoxQ1) and its capacity to function as a competitive endogenous RNA (ceRNA) underscore VCAN’s multifaceted role in creating a pro‐tumorigenic microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nVersican’s function is further refined by precise regulatory and proteolytic mechanisms that tailor its activity in different cellular settings. Transcriptional regulation by p53, as well as myocardin-induced microRNAs (for example, miR-143), modulates VCAN expression during smooth muscle differentiation and influences cell migration. Furthermore, proteolytic processing by ADAMTS family proteases generates bioactive fragments (often referred to as versikine) that can alter inflammatory signaling, activate cytokine production, and influence the fibroblast-to-myofibroblast transition. Such post‐translational modifications and cleavage events not only determine the availability and composition of the extracellular matrix but also have far‐reaching effects on immune cell behavior and the tumor microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "44"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Thomas N Wight, Mervyn J Merrilees "}, {"type": "b", "children": [{"type": "t", "text": "Proteoglycans in atherosclerosis and restenosis: key roles for versican."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Circ Res (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/01.RES.0000126921.29919.51"}], "href": "https://doi.org/10.1161/01.RES.0000126921.29919.51"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "15142969"}], "href": "https://pubmed.ncbi.nlm.nih.gov/15142969"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "John M Norian, Minnie Malik, Candace Y Parker, et al. 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