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MicroRNA-27a and MicroRNA-27b (miR-27a/b) are highly conserved non-coding RNAs that play pivotal roles in the post-transcriptional regulation of gene expression [1]. They belong to the miR-23~27~24 clusters, with miR-27a located on chromosome 19 and miR-27b on chromosome 9 in humans [2]. These microRNAs share a common seed sequence, allowing them to target a similar set of mRNAs involved in diverse biological processes such as cell cycle control, lipid metabolism, and adipocyte differentiation [3]. In clinical contexts, miR-27a/b are frequently dysregulated; they often act as oncomiRs in various cancers, such as breast and gastric cancer, by suppressing tumor suppressor genes like ZBTB10 [4]. Conversely, they play critical roles in metabolic disorders and cardiovascular health by modulating targets like PPAR-gamma and RXR-alpha [5]. Therapeutic strategies focusing on miR-27a/b involve the use of antisense oligonucleotides (antagomirs) to inhibit their over-expression or miRNA mimics to restore lost function [6]. While promising, the development of miR-27-targeted therapies faces challenges regarding tissue-specific delivery and the potential for unintended off-target effects due to the broad range of genes regulated by a single microRNA [7].
MicroRNAs like miR-27a/b function by binding to the 3' untranslated region (UTR) of specific messenger RNAs (mRNAs) through the RNA-induced silencing complex (RISC), leading to translational repression or mRNA degradation, thereby silencing the expression of target genes.
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