{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐503 has emerged as a multifunctional regulatory molecule in both physiological and pathological contexts. In endothelial and differentiating tissues it participates in vascular homeostasis and cell‐cycle control. For example, in pulmonary arterial endothelial cells, decreased miR‐503 (in concert with miR‐424) downstream of apelin deficiency leads to disinhibition of FGF2/FGFR1 signaling and increased endothelial proliferation in pulmonary arterial hypertension."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In skeletal muscle differentiation, induction of miR‐503 (along with miR‐322/424) helps enforce a G1 arrest by post‐transcriptionally downregulating CDC25A, thereby contributing to myoblast differentiation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " In bone homeostasis, miR‐503 is markedly reduced in osteoclast progenitors from postmenopausal osteoporosis patients, and its restoration inhibits RANK‐dependent osteoclastogenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer, miR‐503 functions in a context‐dependent manner, often exerting tumor‐suppressive actions yet also, in select settings, exhibiting oncogenic features. Several studies indicate that miR‐503 suppresses angiogenesis in hepatocellular and other cancers by coordinately down‐regulating potent angiogenic factors such as FGF2 and VEGFA."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " In non‐small cell lung cancer, enforced miR‐503 expression inhibits tumor cell proliferation and metastasis by targeting components of the PI3K/IKK‐β pathway"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ", as well as by directly repressing anti‐apoptotic Bcl‐2 to sensitize cells to cisplatin."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " In endometrioid endometrial cancer, miR‐503 targets cyclin D1 (CCND1) to impair cell‐cycle progression"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ", and similarly in breast cancer, reduced miR‐503 levels correlate with enhanced proliferation by failing to restrain CCND1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " In glioblastoma, diminished miR‐503 facilitates oncogenic insulin‐like growth factor‐1 receptor (IGF‐1R) signaling"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ", whereas in prostate cancer, restoration of miR‐503 (which is suppressed by reduced GATA3 activity) targets oncogenic factors such as ZNF217"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "and RNF31."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " Notably, in colon adenoma progression, cooperative expression of miR‐182 and miR‐503 results in repression of the tumor suppressor FBXW7 and appears to drive malignant transformation"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", while in ovarian cancer the miR‐424/503 cluster suppresses the oncogenic kinesin KIF23 thereby inhibiting cell proliferation and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": " Interestingly, divergent roles have been reported in breast cancer as certain studies describe an overexpressed miR‐503‐3p isoform that promotes epithelial–mesenchymal transition by targeting SMAD2 and reducing E‐cadherin"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ", highlighting that isoform‐ or context‐specific processing may dictate whether miR‐503 acts as a tumor suppressor or a promoter of metastasis.\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, miR‐503 exerts its regulatory functions by targeting an array of mRNAs involved in key cellular processes. Its repertoire of targets includes regulators of cell cycle progression (CDC25A, CCND1, p21), apoptosis (Bcl‐2, PUMA), growth and angiogenesis (FGF2, VEGFA, IGF‐1R), and components of transforming growth factor‐β and NF‐κB signaling (Smad7, Smurf2, as part of the miR‐424/503 cluster)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": " miR‐503 levels are subject to regulation by both epigenetic mechanisms, such as hypermethylation of its promoter in non‐small cell lung cancer"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ", and by interactions with competing endogenous RNAs: long noncoding RNAs like miR503HG in hepatocellular carcinoma synergize with miR‐503 to inhibit metastasis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ", and circular RNAs such as circ‐BANP act as sponges to reduce miR‐503 activity in lung cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": " Furthermore, epigenetic and transcriptional regulation of the broader miR‐424/503 cluster has been linked to TGF‐β–mediated cell cycle arrest in mammary epithelial cells"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": ", and chemotherapeutic agents (e.g. epirubicin) can modulate the exosomal export of miR‐503 through RNA‐binding proteins."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies underscore that miR‐503 is a key post‐transcriptional regulator that modulates cell proliferation, differentiation, apoptosis, angiogenesis, and metastasis in a tissue‐ and context‐dependent manner. Its dysregulation—whether through altered expression, epigenetic silencing, or sequestration by competing RNAs—can contribute to disease states, ranging from vascular dysfunction and impaired myogenesis to various forms of cancer and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}, {"type": "fg_f", "ref": "6"}, {"type": "fg_fs", "start_ref": "22", "end_ref": "28"}]}, {"type": "t", "text": " This diverse regulatory capacity of miR‐503 not only aids our understanding of its contributions to disease pathogenesis but also highlights its potential as a prognostic biomarker and therapeutic target in multiple pathological states.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jongmin Kim, Yujung Kang, Yoko Kojima, et al. 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