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MicroRNA-1825 (miR-1825) is a small non-coding RNA molecule that plays a critical role in the post-transcriptional regulation of gene expression. It functions primarily by binding to the 3' untranslated region (UTR) of target messenger RNAs, leading to translational repression or mRNA degradation [1, 8]. In the context of neurodegenerative diseases, miR-1825 is significantly downregulated in patients with amyotrophic lateral sclerosis (ALS), where it regulates the TBCB/TUBA4A pathway, contributing to motor neuron defects [1, 5]. Conversely, miR-1825 has been shown to promote the proliferation of adult cardiomyocytes and enhance cardiac regeneration following ischemic injury, suggesting a therapeutic role in heart failure [2, 9]. In oncology, its role is context-dependent; it acts as a tumor suppressor in glioblastoma by targeting CDK14, but can promote angiogenesis and metastasis in colorectal cancer through the exosomal miR-1825/ING1/TGF-beta axis [4, 7]. While no specific drugs targeting miR-1825 are currently approved, it is being investigated as a target for miRNA mimics in ALS and cardiac repair, as well as a diagnostic biomarker in various cancers and neurological disorders [3, 11, 13].
Binds to the 3' untranslated region (UTR) of target messenger RNAs (mRNAs) to induce translational repression or mRNA degradation, thereby silencing the expression of specific proteins such as TBCB, CDK14, and ING1 [1, 4, 7].
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