{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‑96 is a multifunctional microRNA whose dysregulation has been implicated in a wide range of human malignancies. In several breast and prostate cancers, increased miR‑96 expression promotes cellular proliferation, invasion, and survival through direct repression of key tumor suppressors such as FOXO1, FOXO3, and RECK. In some contexts, miR‑96 also modulates DNA repair and chemosensitivity by targeting factors including RAD51 and REV1, whereas in non‑small cell lung cancer, exosomal miR‑96 enhances viability, migration, and drug resistance by downregulating targets like LMO7. Conversely, in pancreatic and colorectal cancers, miR‑96 can act in a tumor‑suppressive role by directly targeting KRAS or, in a related mechanism, its suppression by oncogenic factors (e.g., EVI1) drives KRAS upregulation. Additional studies in hepatocellular and esophageal cancers have linked miR‑96 overexpression to reduced apoptosis and enhanced oncogenic signaling, while in bladder cancer its upregulation is associated with increased IRS1 and MAP4K1 expression that supports tumor growth."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumor biology, miR‑96 is critical for normal development and cellular homeostasis. Point mutations within its seed region have been directly linked to autosomal dominant, progressive sensorineural hearing loss due to impaired miR‑96 biogenesis and target regulation. In the hematologic compartment, miR‑96 directly suppresses γ‑globin expression, contributing to the fetal-to‑adult hemoglobin switch, while during neuroectoderm specification it modulates developmental programs via targeting transcription factors such as PAX6. miR‑96 has also been shown to influence hepatic cholesterol metabolism by repressing the scavenger receptor SR‑BI and to regulate autophagy in prostate cancer cells in a dose‑dependent manner."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe regulatory networks governing miR‑96 activity further underscore its contextual complexity. Several long non‑coding RNAs—as exemplified by TP53TG1, GMDS‑AS1, and STXBP5‑AS1—act as competing endogenous RNAs to sequester miR‑96, thereby modulating the expression of key targets such as KRAS, CYLD, and PTEN in pancreatic, lung, and cervical cancers. In addition, upstream signals including TGF‑β and autocrine/paracrine growth hormone signaling can regulate miR‑96 levels, thereby influencing processes like epithelial‑mesenchymal transition and bone metastasis. Moreover, as a member of the evolutionarily conserved miR‑183/96/182 cluster, miR‑96 contributes to dynamic alterations in gene expression that underlie tumor progression and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Irene K Guttilla, Bruce A White "}, {"type": "b", "children": [{"type": "t", "text": "Coordinate regulation of FOXO1 by miR-27a, miR-96, and miR-182 in breast cancer cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M109.031427"}], "href": "https://doi.org/10.1074/jbc.M109.031427"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19574223"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19574223"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Shuangni Yu, Zhaohui Lu, Changzheng Liu, et al. 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