{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐let‑7d exerts multifaceted tumor‐suppressive functions in several cancers. In oral squamous cell carcinoma and renal cell carcinoma, its downregulation is associated with enhanced epithelial–mesenchymal transition, increased migration/invasion and chemoresistance, while experimental overexpression reverses these malignant traits. In ovarian cancer and triple‐negative breast cancer, miR‐let‑7d suppresses cell proliferation, promotes apoptosis and increases chemosensitivity by targeting key oncogenic regulators such as HMGA1, cyclin D1/Akt1/Wnt1 and other effectors. Similarly, in osteosarcoma cancer stem cells, overexpression of miR‐let‑7d reduces stemness and proliferation, albeit sometimes concomitantly enhancing migratory potential, underscoring a context‐dependent dual role in tumor biology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn fibrotic pathologies, miR‐let‑7d plays a key antifibrogenic role. In idiopathic pulmonary fibrosis and related models, reduced miR‐let‑7d levels impair epigenetic gene silencing and promote transforming growth factor‐β–driven epithelial–mesenchymal transition, whereas restoration of miR‐let‑7d expression—as also observed in intrauterine adhesion models where it represses HMGA2—attenuates fibrogenesis and EMT processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMiR‐let‑7d also contributes to the regulation of vascular and metabolic homeostasis. In endothelial cells, its overexpression limits proliferation, migration, and tubulogenesis through direct targeting of IFI44L, while in vascular smooth muscle cells increased miR‐let‑7d levels reduce cell proliferation and inflammatory signaling (notably through NF‑κB attenuation), suggesting a protective role against atherosclerosis. Moreover, its dysregulation has been implicated in metabolic liver disorders such as non‑alcoholic fatty liver disease, highlighting its promise as a circulating diagnostic biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer and vascular regulation, miR‐let‑7d is emerging as a critical modulator in several neurological, autoimmune, and reproductive disorders. Elevated circulating miR‐let‑7d levels have been identified as potential biomarkers in attention‑deficit/hyperactivity disorder, while in fibromyalgia its expression correlates with small nerve fiber loss. In autoimmune conditions such as primary Sjögren’s syndrome, miR‐let‑7d regulates interleukin‑17 expression via AKT1/mTOR signaling. Its aberrant expression in granulosa cells of polycystic ovary syndrome and in trophoblasts of pre‑eclamptic pregnancies further supports roles in modulating cell proliferation, invasion, and apoptosis in reproductive tissues. Moreover, altered miR‐let‑7d levels in Down syndrome and Alzheimer’s disease, among other conditions, underscore its potential as a diagnostic and prognostic blood‑based biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, miR‐let‑7d is embedded in a complex regulatory network responsive to metabolic and hormonal cues. Its transcription is subject to modulation by factors such as MYC, Lin28B, and nutrient signals including glucose and inflammatory cytokines, as demonstrated by promoter analyses. 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