{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑1179 is an evolutionarily conserved microRNA with context‐dependent roles in human diseases. In certain malignancies such as familial breast cancer and esophageal squamous cell carcinoma, miR‑1179 is aberrantly overexpressed, and its elevated levels have been associated with enhanced metastatic potential. In these settings, increased miR‑1179 contributes to tumor progression through the downregulation of key tumor‐suppressive proteins (e.g. BRCA1) or regulators of cell adhesion and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast, in a majority of cancers including non‑small cell lung cancer, gastric cancer, pancreatic cancer, hepatocellular carcinoma, nasopharyngeal carcinoma, and multiple myeloma, miR‑1179 expression is significantly down‑regulated. Functional studies in these contexts have shown that restoring miR‑1179 levels suppresses cell proliferation, migration, and invasion and promotes cell cycle arrest or apoptosis. Mechanistically, miR‑1179 targets various oncogenes such as SPAG5, HMGB1, E2F5, ZEB2, HMGB3, and epiregulin, thereby impeding oncogenic signaling pathways—including Akt activation—and ultimately exerting a tumor‑suppressive effect."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "10"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA recurrent theme in these studies is the regulation of miR‑1179 by competing endogenous RNA (ceRNA) networks. In several cancers and even in non‑neoplastic conditions, specific circular RNAs (circRNAs) and long non‑coding RNAs (lncRNAs) function as molecular sponges that bind and sequester miR‑1179. For instance, in papillary thyroid carcinoma and non‑small cell lung cancer, circRNAs such as hsa_circ_0039411, circ_0062389, circ_0000735, and in ovarian granulosa cells in polycystic ovary syndrome, circ_0043533, as well as lncRNA LINC01929 in NSCLC, have been shown to interact with miR‑1179. This sponging diminishes the availability of miR‑1179 to bind to its targets and thereby modulates downstream oncogenic signaling and disease progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "15"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in cancer, miR‑1179 has been implicated in other pathophysiological contexts. In familial breast cancer with distant metastases, for example, a specific BRCA1 variant (c.2311T>C) in combination with miR‑1179 over‑expression correlates with loss of BRCA1 protein expression and aggressive disease."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In addition, a non‑coding mutation in a thyroid‐specific regulatory element activates the MIR7‑2/MIR1179 locus, resulting in their over‑expression and contributing to resistance to thyroid stimulating hormone."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": " Preliminary investigations into the involvement of miR‑1179 in idiopathic recurrent pregnancy loss and osteoarthritis further underscore its emerging significance across diverse human diseases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Imen Medimegh, Wafa Troudi, Nejla Stambouli, et al. 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