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The miR-27a binding site on the Vascular endothelial cadherin (CDH5) mRNA 3' untranslated region (UTR) is a specific regulatory sequence that mediates the post-transcriptional repression of VE-cadherin expression. VE-cadherin is a transmembrane protein essential for the formation and maintenance of endothelial adherens junctions, which regulate vascular permeability and leukocyte extravasation (UniProt P33151). When miR-27a binds to this site, it inhibits the translation or promotes the degradation of CDH5 mRNA, leading to weakened cell-cell contacts and increased endothelial sprout formation (Young et al., 2013, Blood). This mechanism is frequently exploited in cancer, where upregulated miR-27a promotes tumor angiogenesis and facilitates metastasis by destabilizing the vascular barrier (Zhao et al., 2016, Scientific Reports). Therapeutic strategies focusing on this target include miR-27a antagomirs and site-blocking oligonucleotides (SBOs) designed to prevent the miRNA from accessing this specific UTR sequence, thereby restoring vascular stability.
Post-transcriptional gene silencing of VE-cadherin via mRNA degradation or translational inhibition.
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