{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐455, which exists in both the –3p and –5p forms, has emerged as a multifaceted regulator in cancer. In melanoma, for example, the unedited wild‐type miR‐455‐5p accelerates tumor growth and metastasis by targeting tumor suppressors such as CPEB1, whereas its A‐to‐I RNA–edited counterpart exerts opposite, inhibitory effects."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In medullary thyroid carcinoma, downregulation of miR‐455 is observed, suggesting a potential tumor–suppressive role"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", whereas in colorectal cancer miR‐455 suppresses cell proliferation and invasion via direct regulation of RAF1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Similar tumor–suppressive roles have been described in non–small cell lung cancer, where miR‐455‐3p inhibits proliferation and migration by targeting genes such as HOXB5"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "and ZEB1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " In contrast, studies in oral squamous cell carcinoma report an oncogenic function of miR‐455‐5p that, under transcriptional control of TGF–β/SMAD3, promotes tumorigenesis by downregulating UBE2B"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", while in triple–negative breast cancer, its overexpression enhances invasion and migration through repression of the tumor suppressor EI24."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Additional reports indicate that in prostate, breast, gastric, pancreatic, bladder, hepatocellular, and even skull base chordoma, miR‐455 (whether –3p or –5p) operates by targeting key regulators such as eIF4E"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", CDK14"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ", EGFR"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", and IGF–1R"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": ", while its expression is modulated via competing endogenous RNAs such as DLEU2"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", OXCT1–AS1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", and HOXA–AS3."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " Moreover, analyses of exosomal miR‐455 in breast cancer further support its potential as a diagnostic marker"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "and studies linking GATA3 to miR‐455–3p emphasize its role in suppressing epithelial–to–mesenchymal transition."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‐455 has been implicated in several non–malignant conditions. In Alzheimer’s disease, elevated levels of miR‐455–3p in patient serum, postmortem brains, and various experimental models position it as a promising peripheral biomarker that modulates amyloid precursor protein expression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": " In diabetic nephropathy, miR‐455–3p expression is suppressed in renal cells exposed to high glucose or TGF–β1, and its restoration alleviates extracellular matrix deposition and epithelial–mesenchymal transition via targeted regulation of ROCK2."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": " Its participation in cartilage homeostasis is underscored by findings in chondrogenic differentiation, where miR‐455–3p promotes histone H3 acetylation by targeting HDAC2/8"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": ", while in mechanically stressed endplate chondrocytes, TGF–β/SMAD signaling upregulates miR‐455–5p to suppress RUNX2 and mitigate degeneration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": " In osteoarthritis, aberrant miR‐455–3p activity contributes to chondrocyte apoptosis and inflammation by directly targeting COL2A1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": "and additional studies further reveal its impact on the PI3K/AKT pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": " Similarly, in preeclampsia, downregulation of both miR‐455–3p and miR‐455–5p in placental tissue hints at a disruption of hypoxia signaling and trophoblast differentiation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, the pleiotropic functions of miR‐455 are highly context–dependent. Its expression and activity can be modulated by RNA editing—as evidenced in melanoma—and by competing endogenous RNAs, including various long non–coding RNAs that act as molecular sponges in different tumor types. Through direct binding to the 3′ untranslated regions of diverse target mRNAs (such as those encoding CPEB1, UBE2B, RAF1, HOXB5, eIF4E, CDK14, SMAD2, ROCK2, COL2A1, RUNX2, and IGF–1R), miR‐455 orchestrates a wide range of cellular processes including proliferation, apoptosis, migration, adhesion, and metabolic reprogramming. 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