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lncRNA EGFL7 opposite strand (LNCEGFL7OS) is a primate/human-specific long noncoding RNA located on the opposite strand of the EGFL7/miR-126 gene locus. It is highly enriched in endothelial cells of vascularized tissues and regulated by ETS-family transcription factors via a bidirectional promoter[1][4][5]. LNCEGFL7OS is critical for angiogenesis; its silencing impairs vessel formation and its overexpression promotes angiogenic activity. Mechanistically, LNCEGFL7OS interacts with the MAX transcription factor, modulating histone modifications and the expression of neighboring EGFL7 and miR-126, thus activating signaling pathways essential for endothelial cell function (MAPK, AKT). It also influences proliferation, apoptosis, and migration, particularly in lung adenocarcinoma cells, suggesting an important role in tumorigenesis and cardiovascular disease[1][2][5][4].
Not established for drugs. The molecule itself mediates activation of key signaling pathways (MAPK, AKT) and chromatin modification (histone acetylation via interaction with MAX protein) at the EGFL7/miR-126 locus[1][5].
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