{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐138 (miR‑138), transcribed from the MIR138‑2 locus, plays multifaceted roles in tumor biology as a context‐dependent regulator. In several cancers—including head and neck squamous cell carcinoma, tongue squamous cell carcinoma, chronic myeloid leukemia, non‑small cell lung cancer, ovarian cancer, pancreatic cancer, oral squamous cell carcinoma, Ewing’s sarcoma, glioblastoma, osteosarcoma, colorectal, cervical, breast, prostate, gastric, and melanoma—miR‑138 is frequently downregulated. Its restoration often inhibits tumor cell proliferation, migration, invasion, and epithelial–mesenchymal transition, while promoting cell cycle arrest and apoptosis. Mechanistically, miR‑138 exerts tumor‑suppressive effects by directly targeting a spectrum of oncogenic transcripts (including GNAI2, BCR‑ABL, CCND3, PD‑L1, SIRT1, Limk1, YAP1, ERCC1/ERCC4, FAK, and hTERT), thereby modulating critical signaling pathways such as Wnt/β‑catenin, PI3K/Akt, and TGF‑β. Notably, in certain contexts—such as glioblastoma—miR‑138 overexpression can also confer chemoresistance by attenuating apoptosis and inducing autophagy, highlighting its context‑dependent and sometimes paradoxical functions in cancer progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its established roles in malignancy, miR‑138 is emerging as a pivotal regulator in diverse non‑neoplastic contexts. In cardiomyocytes subjected to chronic hypoxia, miR‑138 upregulation confers protection against apoptosis by targeting MLK3 and modulating downstream JNK/c‑jun signaling. In skin and scar biology, altered miR‑138 levels influence fibroblast function and extracellular matrix remodeling by regulating factors such as PPAR‑β and EZH2, while in articular chondrocytes and bone tissue miR‑138 modulates differentiation and mechanosensitivity through effectors like MACF1. Furthermore, aberrant serum levels of miR‑138 have been linked to metabolic conditions such as obesity and type 2 diabetes mellitus, and in intervertebral disc degeneration, miR‑138‑5p promotes apoptosis via the SIRT1/PTEN/PI3K/Akt axis. Finally, in other settings—including placental function in gestational diabetes, Alzheimer’s disease (where miR‑138 promotes tau phosphorylation via the RARA/GSK‑3β pathway), and even sepsis‑associated acute lung injury where mitophagy and pyroptosis are implicated—miR‑138 stands out as a versatile modulator of cellular stress responses and differentiation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xiqiang Liu, Lu Jiang, Anxun Wang, et al. 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