{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐378a is a multifaceted regulator in cancer, exhibiting context‐dependent dual roles. In several tumor types—including breast, lung, gastric, colorectal, cervical, melanoma, and glioblastoma—miR‐378a influences cell survival, proliferation, migration, invasion, metabolic reprogramming, and angiogenesis. In some settings it exerts oncogenic actions—for example, by enhancing tumor growth and promoting the Warburg effect through suppression of tumor suppressors such as Sufu, Fus‐1, TOB2, and ST7L, or by contributing to chemoresistance via sCLU inhibition and modulation of GOLT1A, MAPK1, and GRB2 signaling. In other contexts, restoration of miR‐378a expression has been shown to trigger cell cycle arrest and apoptosis, inhibit key signaling cascades (e.g. the Wnt/β‐catenin, ERK1/2 and p38 MAPK pathways), and even favor the formation of edited, anti‐metastatic isoforms that target oncogenes like PARVA or TSPAN17. These findings underscore its complex, cell‐ and context‐dependent roles in neoplastic transformation, metastasis and therapeutic response."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumor biology, miR‐378a also orchestrates key processes related to cell differentiation, tissue remodeling and immune regulation. It modulates differentiation in diverse cell types—promoting osteoblast differentiation and bone nodule formation, regulating trophoblast cell proliferation, migration and invasion during placental development, and limiting hepatic stellate cell activation to suppress liver fibrosis and cardiac remodeling. In addition, miR‐378a downregulation in activated natural killer cells helps release cytolytic effectors, while its inhibition in fibroblasts enhances wound healing by de‐repressing targets such as vimentin and integrin‐β₃, and it may also influence adipogenic pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, miR‐378a contributes to metabolic homeostasis and represents a promising circulating biomarker. It is implicated in the regulation of energy balance by modulating adiponectin expression and influencing xenobiotic responses via induction of a miR‐378–recognition site in the aryl hydrocarbon receptor transcript. Its altered levels in serum and exosomes have been linked to several pathologies—including renal cell carcinoma, non–small cell lung cancer and even responses to cancer vaccination—highlighting its potential utility in non‐invasive disease diagnosis and prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Daniel Y Lee, Zhaoqun Deng, Chia-Hui Wang, et al. 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