{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐143 plays a pivotal tumor‐suppressive role in a broad spectrum of human cancers. In colorectal, prostate, bladder, cervical, esophageal, renal, and soft tissue tumors the down‐regulation of miR‐143 has been consistently observed and is associated with increased tumor cell proliferation, migration, invasion, and chemoresistance. Mechanistically, miR‐143 exerts its tumor‐suppressive effects by directly targeting key oncogenic drivers and signaling intermediates—including KRAS, IGF1R, MDM2, ERK5, Akt, BCL2, and metabolic regulators like hexokinase 2—thus attenuating mitogenic and survival cascades. Restoration of miR‐143 expression, for instance using chemically modified mimics, leads to the inhibition of MAPK and PI3K cascades and has been shown to decrease anchorage‐independent growth and induce apoptosis in both in vitro and in vivo models, underscoring its potential as a therapeutic candidate."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its anticancer actions, the miR‐143/145 cluster is integral to vascular biology. In endothelial cells stimulated by atheroprotective flow, miR‐143 is transcriptionally upregulated and packaged into extracellular vesicles, serving as a paracrine mediator to promote a differentiated, contractile phenotype in adjacent vascular smooth muscle cells. Moreover, miR‐143 is upregulated by TGF‐β/BMP and Notch signaling pathways in vascular smooth muscle cells, where it contributes to the suppression of negative regulators (such as KLF4) to reinforce proper contractile gene expression and vascular tone. These mechanisms are essential for maintaining vascular homeostasis and protecting against atherosclerotic lesion formation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumor suppression and vascular regulation, miR‐143 is implicated in diverse processes such as metabolic reprogramming and immunomodulation. By targeting glycolytic enzymes like HK2, miR‐143 counteracts the Warburg effect in cancer cells and modulates energy metabolism. Its expression is finely regulated by inflammatory signals and long non‐coding RNAs, and in some contexts—even in hepatocellular and gastric cancers—altered miR‐143 levels can influence epithelial–mesenchymal transition and metastasis. Furthermore, in mesenchymal stem cells, miR‐143 modulates immunosuppressive pathways by targeting kinases within inflammatory signaling cascades. Collectively, these studies reveal the multifaceted functions of miR‐143 in integrating oncogenic, metabolic, and inflammatory cues across pathological and physiological settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "X Chen, X Guo, H Zhang, et al. 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