MicroRNA 126 (miR-126)

MicroRNA 126 (miR-126) is a short, non-coding RNA molecule classified as a microRNA, primarily expressed in endothelial cells where it plays a critical role in controlling angiogenesis (the formation of new blood vessels), vascular integrity, and the maintenance of endothelial phenotype[1][3][5]. Encoded within the 7th intron of the EGFL7 gene on human chromosome 9, miR-126 modulates gene expression at the post-transcriptional level by binding target mRNAs, leading to their repression or degradation[2]. Its direct targets include crucial regulators of vascular signaling and integrity such as SPRED1, PIK3R2, VCAM-1, and EGFL7, thus modulating VEGF and MAP kinase pathways[3][5]. miR-126 acts as both a tumor suppressor and, contextually, as an oncogene in various cancers by suppressing genes involved in cell proliferation, migration, invasion, and angiogenesis[1]. Reduced miR-126 levels are observed in multiple cancer types, and manipulation of its expression has been used to alter tumor aggressiveness, especially in B-acute lymphoblastic leukemia (B-ALL)[4]. Additionally, miR-126 is implicated in inflammatory and cardiovascular conditions, serving as a potential biomarker for non-invasive diagnosis and prognosis[1][2]. No drugs directly target miR-126 clinically, but modulating its function experimentally via mimics or inhibitors is under research. Safety concerns for therapeutic strategies include the risk of disrupting vascular homeostasis.

Other names

hsa-miR-126MIRN126miRNA126mir-126MIR126*

Post-transcriptional repression of target mRNAs (by base-pairing with 3' UTR, leading to translational inhibition or mRNA degradation); Inhibition of negative regulators of VEGF signaling (e.g., SPRED1, PIK3R2)