{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence indicates that microRNA‑542 (including both the ‑3p and ‑5p forms) plays multifaceted roles in human disease, particularly in cancer. In several solid tumors such as breast, neuroblastoma, melanoma, ovarian, gastric, colorectal, esophageal and lung cancers, miR‑542 has been shown to act predominantly as a tumor suppressor by directly binding to the 3′‑untranslated regions of key pro‑tumorigenic mRNAs. This results in impaired translation of genes involved in angiogenesis (e.g. Angiopoietin‑2), cell cycle progression and apoptosis inhibition (e.g. Survivin), Wnt signaling (via FZD7), oncogenic kinases (e.g. PIM1 and CDK14) and cytoskeletal regulators (e.g. cortactin), as well as by enhancing p53 protein stability. In these studies the enforced expression of miR‑542‑3p inhibited tumor cell proliferation, migration, invasion and metastasis, and improved sensitivity to anticancer agents, thereby supporting its potential as both a prognostic biomarker and therapeutic target in diverse malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to these tumor‐suppressive functions, mechanistic studies have uncovered that miR‑542 modulates several critical signaling pathways that govern cellular homeostasis and therapeutic response. For example, miR‑542 has been implicated in the regulation of p53 stability through interference with its negative regulators, modulation of the PI3K/AKT and β‑catenin pathways, and interference with Ras/FAK/c‑Src circuits. In certain contexts, such as tamoxifen‑resistant breast cancer and some osteosarcoma models, alterations in miR‑542 (including upregulation of the ‑5p arm) correlate with deregulated survival signaling, altered autophagy and aberrant mitochondrial function. Moreover, miR‑542 can be influenced by upstream factors such as tumor‑derived angiogenin or long noncoding RNAs that serve as competing “sponges,” thereby affecting its bioavailability and downstream impact on oncogenic targets. These findings underscore the complex, context‑dependent role of miR‑542 in modulating oncogenic signaling and drug sensitivity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in oncogenesis and therapeutic response, miR‑542 also contributes to the regulation of non‑malignant processes. In reproductive biology, for instance, overexpression of miR‑542‑3p impairs endometrial decidualization by targeting mRNAs such as IGFBP1 and components of the ILK/TGF‑β1/SMAD2 axis. Furthermore, miR‑542 dysregulation is associated with altered muscle physiology in chronic obstructive pulmonary disease, defective autophagic responses in cardiomyocytes under hypoxia/reoxygenation stress, and even aberrant apoptosis in retinal pigment epithelial cells implicated in diabetic retinopathy. Additional studies have also linked changes in miR‑542 levels with modulation of gene expression during skin differentiation and fibrosis. Collectively, these findings highlight miR‑542’s central role as a fine‑tuner of gene networks that govern cell proliferation, differentiation, survival and tissue homeostasis in both pathological and physiological settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "37", "end_ref": "41"}, {"type": "fg_f", "ref": "20"}, {"type": "fg_f", "ref": "42"}, {"type": "fg_f", "ref": "9"}, {"type": "fg_f", "ref": "43"}, {"type": "fg_f", "ref": "22"}, {"type": "fg_f", "ref": "44"}, {"type": "fg_fs", "start_ref": "23", "end_ref": "25"}, {"type": "fg_f", "ref": "10"}, {"type": "fg_f", "ref": "26"}, {"type": "fg_f", "ref": "28"}, {"type": "fg_f", "ref": "13"}, {"type": "fg_f", "ref": "30"}, {"type": "fg_f", "ref": "45"}, {"type": "fg_f", "ref": "32"}, {"type": "fg_f", "ref": "34"}, {"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Sena Yoon, Young-Chul Choi, Suman Lee, et al. 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