{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐217 is emerging as a pleiotropic regulator in both normal physiology and disease. In non‐malignant contexts, it has been shown to affect vascular and metabolic homeostasis. For example, miR‐217 is up‐regulated in aging endothelial cells where it suppresses the expression of SirT1—a key longevity regulator—thereby contributing to endothelial dysfunction (1). In hepatocytes, chronic ethanol exposure induces miR‐217 expression, which impairs SIRT1 and lipin‐1 function and promotes hepatic fat accumulation, while miR‐217 also participates in the post‐transcriptional downregulation of HO‐1 under hemin exposure (6, 10). In addition, miR‐217 contributes to the regulation of epithelial phenotypes and immune responses as evidenced in pancreatic and viral contexts, and its elevated serum levels have been correlated with diabetic kidney disease progression through modulation of angiogenic and inflammatory mediators (9, 13, 17, 29)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn numerous malignancies—including pancreatic, lung, gastric, renal, and other cancers—miR‐217 frequently functions as a tumor suppressor. Down‐regulation of miR‐217 is associated with derepression of several oncogenic targets such as KRAS, EZH2, E2F3, and others, which in turn fuels proliferation, invasion, metastatic spread, and even chemoresistance. Studies have demonstrated that restoring miR‐217 levels suppresses cancer cell growth and enhances sensitivity to antineoplastic agents through inhibition of key signaling pathways including MAPK and inflammatory cascades (2, 3, 12, 14, 15, 21, 22, 23, 24, 25, 27, 28, 33, 34, 37, 40, 44, 45, 47). Notably, however, select contexts such as hepatocellular carcinoma and HIV‐1 infection have revealed that aberrant increases in miR‐217 can promote aggressive features by modulating cancer stem cell properties and potentiating viral gene expression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "26"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdding further complexity to its functions, miR‐217 is subject to tight regulation by diverse noncoding RNA networks that act as competing endogenous RNAs (ceRNAs). Long noncoding RNAs and circular RNAs – including MALAT1, CRNDE, HOTAIR, KCNQ1OT1, circRNA_100284, circ‐ADAM9, and others – sequester miR‐217, thereby abrogating its repressive effects on targets such as TCF7L2, RUNX2, FOXP1, DKK1, and GRHL2. These ceRNA interactions modulate the Wnt/β‐catenin, JAK/STAT, and other critical signaling pathways involved in tumorigenesis, differentiation, inflammatory responses, and even stem cell maintenance (4, 5, 7, 8, 11, 16, 18, 19, 20, 26, 30, 31, 32, 35, 36, 38, 39, 41, 42, 43, 46, 48). In both malignant and non‐malignant settings, the disruption of the miR‐217 regulatory axis has been linked to altered cell fate decisions, aberrant differentiation (as seen in osteonecrosis, psoriasis, and tendon aging), and modifications in drug sensitivity, underscoring the therapeutic potential of modulating miR‐217 and its interacting network."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "39"}, {"type": "fg_f", "ref": "20"}, {"type": "fg_fs", "start_ref": "40", "end_ref": "47"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Rossella Menghini, Viviana Casagrande, Marina Cardellini, et al. 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