{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐126 is an endothelial‐enriched microRNA processed from an intron of the EGFL7 gene that plays a pivotal role in maintaining vascular integrity and modulating angiogenesis. It is induced by key transcription factors—such as Ets‐1 and Ets‐2—that promote its expression in endothelial cells, where miR‐126 not only limits vascular inflammation by suppressing adhesion molecules like VCAM‐1 but also targets central angiogenic mediators such as VEGF‐A and the PI3K regulatory subunit PIK3R2. Notably, while its actions in endothelial cells are well established, its function in smooth muscle cells remains to be clarified."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a variety of malignancies—including lung, colon, gastric, pancreatic, and breast cancers—miR‐126 commonly exhibits reduced expression, and its restoration exerts potent tumor‐suppressive effects. In lung cancer, miR‐126 diminishes oncogenic signals by targeting the adaptor protein Crk"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "and by down‐regulating VEGF‐A"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", whereas in colon cancer re‐expression of miR‐126 curtails cell proliferation through suppression of p85β and subsequent attenuation of PI3K/AKT signaling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " In breast cancer, enforced miR‐126 levels promote cell cycle arrest via targeting IRS‐1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", and in small cell lung cancer, miR‐126 limits proliferation by directly repressing SLC7A5."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": " In pancreatic cancer, by targeting ADAM9"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "and in metastatic breast cancer by inhibiting pro‐angiogenic factors such as IGFBP2, PITPNC1, and MERTK"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "and"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", miR‐126 limits tumor invasiveness and metastatic colonization. Furthermore, in non‐small cell lung cancer, its re‐expression enhances chemosensitivity by down‐regulating VEGF‐A and MRP1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", and in acute myeloid leukemia miR‐126 helps preserve stem cell quiescence and contributes to chemotherapy resistance via modulation of PI3K/AKT/mTOR signaling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " In addition, circulating miR‐126 has emerged as a promising noninvasive biomarker for colorectal cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinical studies have demonstrated that miR‐126 levels in the circulation serve as key indicators of endothelial health and metabolic status. Reduced circulating miR‐126 is associated with impaired endothelial progenitor cell function and heightened adipose inflammation in individuals with type 2 diabetes mellitus, pre‐diabetic states, and obesity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "24"}]}, {"type": "t", "text": " Moreover, diminished miR‐126 is detected in acute myocardial infarction and is linked to adverse post‐ischemic cardiac remodeling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nmiR‐126 is also efficiently packaged into extracellular vesicles—including endothelial microparticles and exosomes—thereby mediating critical paracrine signaling in tissue repair and tumor microenvironment modulation. Circulating pro‐angiogenic cell subsets express and secrete high levels of miR‐126, which help potentiate angiogenesis, while platelet‐derived microparticles transfer functional miR‐126 to macrophages to reprogram them toward an enhanced phagocytic, anti‐inflammatory phenotype."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its well‐established roles in the vasculature and in modulating tumor cell behavior, miR‐126 contributes to the regulation of hematopoietic stem cell quiescence and influences chemoresistance in acute myeloid leukemia, while its tissue‐restricted expression is exemplified by the inherently low levels in prostate epithelial cells due to silencing of its host gene—a contrast that may contribute to pro‐migratory phenotypes in these cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}, {"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tamia A Harris, Munekazu Yamakuchi, Marcella Ferlito, et al. 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