{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐1–2 (miR‐1) is a highly conserved, muscle‐enriched regulatory RNA that has emerged as a critical tumor suppressor in a wide variety of solid malignancies. In cancer cells, reduced miR‐1 expression leads to deregulated glucose metabolism through reprogramming of the pentose phosphate pathway, enhanced proliferation and resistance to apoptosis, and increased tumor aggressiveness and metastasis. For instance, miR‐1 downregulation has been shown to promote oncogenic metabolic flux by enhancing the expression of pentose phosphate pathway genes, while its restoration decreases NADPH production, ribose synthesis, and in vivo tumor growth."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In addition, miR‐1 processing is perturbed in myotonic dystrophy, leading to dysregulation of key cardiac transcripts and contributing to heart dysfunction"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", and its interaction with long non‐coding RNAs such as MALAT1 and UCA1 has been implicated in modulating cell migration, invasion, cancer stem cell activity, and radioresistance in breast, nasopharyngeal, gallbladder, bladder, and other cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "5"}]}, {"type": "t", "text": " Furthermore, miR‐1 suppresses breast cancer stem cell stemness via down‐regulation of components in the Wnt/β‐catenin pathway"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", induces apoptosis in nasopharyngeal carcinoma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ", and its consistent downregulation in colorectal, non–small cell lung, chordoma, mesothelioma, glioblastoma, ovarian cancer, osteosarcoma, renal cell carcinoma, hepatocellular carcinoma, uterine leiomyosarcoma, and esophageal cancer correlates with poor clinical outcome."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the cardiovascular system, miR‐1 plays a dual role. On one hand, altered miR‐1 expression modulates myocardial bioenergetics, electrical conduction, and cell survival, acting as a sensitive circulating biomarker for cardiac injury, acute myocardial infarction, and doxorubicin‐induced cardiotoxicity"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "26"}]}, {"type": "t", "text": " miR‐1 levels correlate with troponin rise and changes in left ventricular function during cardiopulmonary bypass as well as in postmortem myocardial samples, highlighting its clinical diagnostic value."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": " Moreover, miR‐1 dysregulation contributes to arrhythmogenesis by affecting ion channel expression and modifying gap junction proteins, and its aberrant expression is linked to postoperative atrial fibrillation and abnormal conduction"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "31"}]}, {"type": "t", "text": " miR‐1 is also implicated in the regulation of tumor endothelial cells in hepatocellular carcinoma and serves as a diagnostic adjunct in pediatric viral myocarditis, while altered miR‐1 expression due to myotonic dystrophy and its consequent impact on targets such as gap junction proteins further underscore its importance in cardiac structural and functional integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "32", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer and the heart, miR‐1–2 is a key regulator of muscle differentiation, autophagy, and cellular stress responses. 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