{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‑93, a key member of the miR‑106b‑25 cluster, has emerged as a multifunctional regulator in cancer biology. In several tumor types such as gastric, breast, hepatocellular, lung, ovarian, and adult T‑cell leukemia, miR‑93 exerts oncogenic activities by directly modulating critical cell cycle and survival regulators. For instance, it forms a negative feedback loop with E2F1 and disrupts TGF‑β tumor suppressor signaling by repressing p21 and Bim, while in glioblastoma and hepatocellular carcinoma its overexpression promotes proliferation, migration, and invasion by targeting tumor suppressors including PTEN, CDKN1A, FUS1, and LATS2. Furthermore, by directly suppressing targets such as the integrin‐β8 and DAB2 genes or by modulating the c‑Met/PI3K/AKT pathway, miR‑93 also contributes to enhanced tumor angiogenesis, metastasis, and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its direct oncogenic roles, miR‑93 modulates cellular processes that influence the tumor microenvironment and therapeutic response. It has been implicated in immune evasion by downregulating sensors such as cGAS via targeting epigenetic regulators, and in glioblastoma stem-like cells, it coordinates autophagy by concurrently repressing multiple autophagy regulators (e.g. BECN1, ATG5, ATG4B, SQSTM1/p62). Beyond cancer, miR‑93 is involved in metabolic regulation in non‐malignant contexts; its upregulation in adipose tissue links to insulin resistance in PCOS by directly targeting GLUT4, and in osteoblasts, miR‑93 modulates mineralization through a feedback loop with the transcription factor Sp7. In colorectal cancer, miR‑93 influences radiosensitivity via an ATG12‐mediated autophagy axis, while in lung cancer it promotes epithelial–mesenchymal transition (EMT) through inhibition of NEDD4L."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, miR‑93’s versatility is underscored by its circulating biomarker potential and its regulation via interactions with long non‑coding and circular RNAs. In lung adenocarcinoma, for example, circCRIM1 acts as a sponge for miR‑93, thereby relieving its inhibition of tumor suppressors like the leukemia inhibitory factor receptor. In non‑small cell lung cancer, miR‑93 targets genes such as β‑TRCP2 to enhance Snail expression and promote migration, while in gastric cancer it downregulates IFNAR1, activating STAT3 and further promoting metastasis. 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