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hsa-miR-20a-3p is a mature microRNA molecule derived from the miR-17~92 cluster, a highly conserved polycistronic miRNA group located on human chromosome 13 [6]. It functions as a critical post-transcriptional regulator of gene expression by binding to the 3' untranslated regions (UTRs) of target messenger RNAs, leading to their degradation or translational repression [6, 10]. This microRNA is involved in a wide array of biological processes, including the regulation of the cell cycle, apoptosis, and mitochondrial dynamics [1, 2]. In the context of disease, hsa-miR-20a-3p exhibits a dual role; it has been identified as a neuroprotective agent in ischemic stroke by modulating astrocytic and neuronal survival and reducing neuroinflammation [1, 2]. Conversely, it often acts as an oncomir in various cancers, such as breast, lung, and colorectal cancer, where its overexpression correlates with poor prognosis, epithelial-mesenchymal transition (EMT), and drug resistance [3, 4, 5]. Therapeutic development focuses on using synthetic mimics to enhance its protective effects in neurological disorders or antagomirs to silence its oncogenic activity in tumors [1, 7, 10]. However, the clinical translation of miR-20a-3p-targeted therapies faces significant hurdles, including the risk of off-target effects due to the large number of genes regulated by a single miRNA and the need for efficient, tissue-specific delivery systems [7, 12].
RNA interference (RNAi) mediated by the RNA-induced silencing complex (RISC), leading to translational inhibition or mRNA degradation of target genes such as PCK1, COL11A1, and various matrix metalloproteinases [1, 5, 6].
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