{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐151A is subject to post‐transcriptional modification that can profoundly influence its biogenesis. For example, adenosine‐to‐inosine editing within the primary transcript of miR‐151 completely blocks its processing by Dicer, resulting in the accumulation of its precursor and thereby altering its maturation (​."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn various cancers the expression and activity of miR‐151A isoforms have been linked to aggressive tumor behavior. In hepatocellular carcinoma, amplification of miR‐151 (often expressed with its host gene FAK) promotes intrahepatic metastasis by targeting RhoGDIA and thereby activating Rho GTPases. Similarly, in breast cancer and head and neck squamous cell carcinoma, miR‐151A (in its –3p and –5p forms) modulates metastasis by regulating key mediators such as TWIST1, SMARCA5, and LYPD3. In glioblastoma and other gliomas, reduced miR‐151A levels are associated with enhanced DNA repair via XRCC4 and, conversely, its activity (or loss thereof) influences migration through targeting ARHGDIA. In prostate, lung, colorectal, gastric, ovarian cancers, and osteosarcoma, aberrant expression of miR‐151A promotes proliferation, epithelial–mesenchymal transition and invasion by acting on distinct targets – including NEK2, AGMAT, and through interactions with non‐coding RNAs (for instance, circular RNAs such as circ_0000073 and circ_0007841, as well as lncRNAs like LINC01123) that modulate its bioavailability. Moreover, miR‐151A can be delivered via exosomes to reprogram the tumor microenvironment, as observed in gastric cancer where exosomal miR‐151A–3p induces Kupffer cell transformation and macrophage M2 polarization, thus facilitating liver metastasis. In addition, circulating levels of miR‐151A have been explored as minimally invasive biomarkers in metastatic castration‐resistant prostate cancer (mCRPC) (via plasma profiling) and in other clinical settings (including lung cancer) (​."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‐151A plays roles in several non‐neoplastic conditions. In the context of reproductive physiology, increased seminal plasma miR‐151A–5p has been linked to decreased mitochondrial respiratory activity and reduced ATP production in severe asthenozoospermia, suggesting a role in sperm viability. Its dysregulation has also been implicated in immune and inflammatory conditions: elevated circulating miR‐151A–3p has been observed in myasthenia gravis and atopic dermatitis, where it modulates targets such as IL12RB2. Furthermore, altered levels of miR‐151A have been reported in acute cardiovascular events – for instance, its early elevation in plasma has been associated with ST‐segment–elevation myocardial infarction, possibly reflecting plaque rupture – and in skeletal homeostasis, where overexpression in adolescent idiopathic scoliosis appears to disturb bone metabolism via inhibition of GREM1 (​."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yukio Kawahara, Boris Zinshteyn, Thimmaiah P Chendrimada, et al. 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