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miR-27a binding site on Vascular endothelial cadherin mRNA 3' untranslated region

Molecular classification
RNA, MicroRNA binding site, Non-coding regulatory element
01

Overview

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.

Other names
miR-27a binding site on CDH5 mRNAmiR-27a-3p target site on VE-cadherinVascular endothelial cadherin 3' UTR miR-27a site
02

Mechanism of action

Post-transcriptional gene silencing of VE-cadherin via mRNA degradation or translational inhibition.

03

Biological functions

Regulation of gene expressionEndothelial cell-cell adhesionVascular permeabilityAngiogenesis
04

Disease associations

CancerCardiovascular diseaseInflammationAtherosclerosis
05

Safety considerations

Off-target effects on other miR-27a targetsSystemic vascular leakageImpaired wound healing
06

Interacting drugs

miR-27a inhibitors

2 more in the full profile.

07

Biomarkers

miR-27a expression levelsVE-cadherin protein levelsVascular permeability markers

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