{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐579-3p has emerged as a pivotal tumor‐suppressive microRNA in several cancers. In melanoma, reduced levels of miR‐579-3p correlate with poor patient survival and the development of resistance to targeted therapies by de‐repressing oncogenic drivers such as BRAF and MDM2. In glioblastoma, enforced expression of miR‐579 leads to significant suppression of cell proliferation and migration by directly targeting key members of the PI3K/AKT cascade (mTOR, Rheb, and PDK1), while in hepatocellular carcinoma early downregulation of miR‐579-3p results in enhanced PIK3CA/AKT signaling that promotes tumor cell proliferation and migration. Additionally, a regulatory axis involving circBCL11B, miR‐579, and LASP1 has been uncovered in oral squamous cell carcinoma, further substantiating its role in modulating tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its tumor‐suppressive roles in established cancers, miR‐579-3p is intricately involved in mechanisms regulating treatment resistance and gene expression control. In prostate cancer, for example, abiraterone treatment leads to downregulation of miR‐579-3p, which in turn results in increased expression of the androgen transporter SLCO1B3—a contributor to therapy resistance. In osteoblasts, the cPWWP2A circular RNA normally acts as a sponge for miR‐579; when this regulatory buffering is disrupted, miR‐579 accumulates and exacerbates dexamethasone-induced cytotoxicity through the repression of protective targets such as SIRT1 and PDK1. Similar investigations in squamous cell lung carcinoma are beginning to delineate its potential role in oncogenesis while in silico studies indicate that alternative polyadenylation may fine-tune the negative feedback imposed by intronic miR‐579 on its host gene."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nOutside the realm of cancer, miR‐579-3p is implicated in the regulation of neuropsychiatric processes and may serve as a non‐invasive biomarker in inflammatory diseases. Genetic variations upstream of the MIR579 gene modulate its promoter activity and have been linked to altered noradrenergic signaling in panic disorder, influencing defensive responses and peripheral cardiovascular parameters during anxiety-provoking situations. Moreover, profiling of plasma-derived extracellular vesicles has revealed that aberrant expression of miR‐579-3p is associated with chronic pancreatitis and even distinguishes subgroups of patients with pre-diabetic features, underscoring its potential utility as a diagnostic tool."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Luigi Fattore, Rita Mancini, Mario Acunzo, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "The effect of miR-579 on the PI3K/AKT pathway in human glioblastoma PTEN mutant cell lines."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Cell Biochem (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/jcb.28935"}], "href": "https://doi.org/10.1002/jcb.28935"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31243804"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31243804"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Wei Zeng, Mengmeng Guo, Lin Yao, et al. 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