{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nResearch across multiple human malignancies indicates that miR‑383 is frequently downregulated in tumor tissues compared with their normal counterparts. In studies of testicular maturation arrest, medulloblastoma, and glioma, diminished miR‑383 levels were associated with aberrant cell proliferation, defective cell cycle regulation, and impaired apoptosis."}, {"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": "\nAt the molecular level, miR‑383 exerts its tumor‐suppressive functions by directly targeting a range of oncogenic drivers and cell‐cycle regulators. For example, in different tumor settings its actions include downregulation of transcription factors and metabolic enzymes such as IRF1, PRDX3, TRIM27, LDHA, Cyclin E2, EPAS1, and CREPT; in prostate cancer, reduction of CD44 expression by miR‑383 underlies a decrease in tumor‐initiating potential, while in hepatocellular carcinoma and non‐small cell lung cancer its targeting of key mediators like APRIL and EPAS1 has been linked to reduced proliferation and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional investigations reveal that miR‑383 also modulates drug responsiveness, DNA damage repair, and cellular metabolism. In hepatocellular carcinoma, for instance, miR‑383 targeting of EIF5A2 enhances chemosensitivity, while in testicular carcinoma cells it inhibits H2AX phosphorylation via PNUTS downregulation. 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