{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐92a (including its isoforms miR‐92a‐3p and miR‐92a‐2‐5p) emerges as a multifunctional regulator in oncogenesis. In several studies, elevated levels of miR‐92a in tumor cells and derived exosomes were found to drive epithelial–mesenchymal transition, proliferation, and invasion in diverse cancers such as hepatocellular carcinoma, cervical cancer, osteosarcoma, glioblastoma, gastric cancer, non‐small cell lung cancer, colorectal cancer, breast cancer, liver cancer, and prostate cancer. Mechanistically, miR‐92a exerts its oncogenic influence by targeting tumor suppressors including PTEN, FBXW7, KLF2, KLF4, LRIG1, and WWOX—thereby modulating critical signaling pathways (for example, the Akt/Snail and PI3K/Akt cascades) that underlie tumor progression and metastasis. In addition, its elevated plasma or tissue expression has been correlated with poor clinical outcome, underscoring its potential as a prognostic biomarker in cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in malignant transformation, miR‐92a contributes to vascular and inflammatory pathologies. In vascular disease models, altered expression of miR‐92a modulates endothelial cell proliferation, migration, and repair, with its inhibition promoting re‐endothelialization and reducing neointimal formation following injury. Similarly, elevated miR‐92a levels have been associated with hypertension, arterial stiffness, and atherosclerosis, while in lipopolysaccharide‐stimulated pulmonary endothelium, targeting miR‐92a improved barrier function and reduced inflammatory cytokine release. Moreover, aberrant miR‐92a expression has been implicated in non‐malignant conditions such as cancer‐associated cachexia, endometriosis (via suppression of PTEN and subsequent progesterone resistance), and even autoimmune and neurodegenerative contexts including central nervous system autoimmunity and amyotrophic lateral sclerosis—highlighting its extensive impact on tissue homeostasis and inflammation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies emphasize the significance of miR‐92a as an extracellular communicator and diagnostic tool. Its presence in exosomes mediates cross‐talk between cancer cells and stromal components—facilitating pre‐metastatic niche formation (for instance, via hepatic stellate cell activation) and promoting angiogenesis through partial endothelial–mesenchymal transition. Furthermore, circulating and even stool levels of miR‐92a have shown promising diagnostic performance for early tumor detection in hepatocellular carcinoma, colorectal cancer, and gastric cancer. These findings collectively reveal that miR‐92a not only drives pathogenesis in a wide range of cancers and vascular disorders but also offers clinical utility as a noninvasive biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Chuanyi Zhou, Liangfang Shen, Lei Mao, et al. 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