{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐128–2 (miR‑128–2) emerges as a pivotal regulator in cancer biology by modulating chemoresistance, metastasis, and drug metabolism. In non–small cell lung cancer (NSCLC) cells, high levels of miR‑128–2 have been shown to promote epithelial–mesenchymal transition and stemness through the downregulation of multiple inhibitors of the Wnt/β‑catenin and TGF‑β pathways, thus contributing to chemoresistance and metastatic spread. Mutant p53 isoforms can trigger miR‑128–2 expression, which in turn post‑transcriptionally targets regulators such as E2F5 to impair apoptosis and enhance cisplatin, doxorubicin, and 5‑fluorouracil resistance. In neuroblastoma, increased miR‑128 expression reduces migratory potential by suppressing proteins such as Reelin and DCX. In acute lymphoblastic leukemia, decreased or mutated miR‑128 levels have been linked to glucocorticoid resistance, while in hepatocellular carcinoma miR‑128–3p directly targets CYP2C9 to modulate drug metabolism. Moreover, miR‑128–2 also exerts control over cellular cholesterol homeostasis by downregulating key efflux transporters, contributing further to its multifaceted role in cancer modulation."}, {"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": "\nBeyond chemoresistance, miR‑128–2 significantly influences tumor progression, angiogenesis, and stem cell–like features across a spectrum of malignancies. In glioblastoma, its overexpression limits cell invasion and cooperates with other miRNAs to enhance temozolomide sensitivity. In gastric and colorectal cancers, miR‑128–2 directly targets angiogenic factors such as VEGF‑C and participates in competitive endogenous RNA networks involving oncogenic long non‑coding RNAs—including PVT1 and SNHG22—which modulate downstream effectors like E2F3. Its dysregulation is also evident in head and neck squamous cell carcinoma and anaplastic thyroid cancer, where reduced miR‑128–2 levels correlate with enhanced proliferation and migration. In breast and pancreatic cancers, diminished miR‑128–2 expression is associated with increased levels of oncogenic targets such as NEK2 and further influenced by regulatory cascades involving kinases like AurkA, while in ovarian cancer it modulates VEGFA‑dependent signaling that affects both cancer stem cell properties and antitumor immunity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies have uncovered roles for miR‑128–2 that extend into metabolic regulation, immune modulation, and even control of genomic stability. In Alzheimer’s disease, upregulation of miR‑128 impairs lysosomal enzyme expression, compromising amyloid‑β clearance. In prostate and laryngeal cancers, miR‑128–2 participates in metabolic reprogramming via pathways involving SNAIL and downstream kinases, while its circulating levels serve as prognostic biomarkers in prostate cancer and hepatocellular carcinoma. By targeting factors such as hnRNP A1, miR‑128–2 helps restrict LINE‑1 retrotransposition, thereby protecting genomic integrity. Furthermore, in inflammatory diseases such as asthma, miR‑128–2 alleviates airway inflammation by modulating mitochondrial dynamics through the downregulation of SIX1, and it also influences tumor immune landscapes—for example, by regulating IL‑16 and T‑cell infiltration. Emerging evidence even suggests a role in regulating EGFR expression in NSCLC and potential links to multiple sclerosis, underscoring the broad regulatory spectrum of this multifaceted miRNA."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Cristina Evangelisti, Maria Carolina Florian, Isabella Massimi, et al. 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