{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR1‐1 is a muscle‐ and heart‐specific microRNA that plays a pivotal role in cardiovascular physiology and pathology. In the failing heart, MIR1‐1, along with other cardiac microRNAs, contributes to the remodeling process and to the reactivation of fetal gene programs, while its circulating levels become altered in acute myocardial infarction and doxorubicin‐induced cardiotoxicity. Moreover, MIR1‐1 is induced during muscle cell differentiation and is modulated by key transcriptional co‐factors such as myocardin, with its altered abundance leading to slowed cardiac conduction, increased arrhythmogenic potential, and impairment of contractility. Its regulation is also intricately linked to post‐transcriptional editing mechanisms in conditions such as myotonic dystrophy, and its expression correlates with key electrophysiological regulators such as hyperpolarization‐activated cyclic nucleotide‐gated channels and fibrotic pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the oncological arena, MIR1‐1 frequently exhibits reduced expression across a spectrum of human cancers – including prostate, lung, gallbladder, breast, nasopharyngeal, esophageal, colorectal, head and neck, chordoma, and osteosarcoma – where it functions as a potent tumor suppressor. Restoration of MIR1‐1 expression in these contexts impairs cell proliferation, migration, invasion, and disrupts cell cycle progression by directly targeting key oncogenic factors (such as MET, Slug, and CORO1C) and by dampening pathways like Wnt/β‐catenin signaling. In addition, MIR1‐1 is embedded in reciprocal regulatory networks with long non‐coding RNAs (for example, MALAT1 and UCA1), which reinforce its tumor‐suppressive functions and affect cellular epithelial–mesenchymal transition and stemness. Its consistent downregulation not only portends poor clinical outcomes and disease recurrence but also renders it a promising diagnostic biomarker and therapeutic target in diverse malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in mature tissues, MIR1‐1 is intricately regulated during development and in response to therapeutic stimuli. Epigenetic alterations such as hypermethylation of its genomic cluster have been associated with diminished expression in colorectal and other cancers, while transcriptional and post‐transcriptional mechanisms further fine‐tune its abundance in diverse cellular contexts. In addition, MIR1‐1 has been shown to promote apoptosis – as observed in nasopharyngeal carcinoma models – and to enhance chemosensitivity in drug‐resistant non‐small cell lung cancer and osteosarcoma cells by modulating targets involved in autophagy and survival signaling. These findings, together with observations in gastric carcinogenesis, underscore the broad regulatory impact of MIR1‐1 on cellular homeostasis and highlight its potential as a molecular biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Thomas Thum, Paolo Galuppo, Christian Wolf, et al. 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