{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n FGD5‐AS1 is a long noncoding RNA that has emerged as a multifaceted regulator in both malignant and non‐malignant disorders. In several cancer types—including colorectal, non‐small cell lung, oral, glioblastoma, renal, cervical, gastric, pancreatic, hepatocellular, ovarian, melanoma, and osteosarcoma—FGD5‐AS1 is frequently upregulated and acts as an oncogene by enhancing cell proliferation, migration, invasion, epithelial–mesenchymal transition, and chemoresistance. Mechanistically, it serves primarily as a competing endogenous RNA (ceRNA) by “sponging” specific microRNAs (e.g. miR‐302e, miR‐107, miR‐520b, miR‐142‐3p, miR‐140‐5p, miR‐153‐3p, miR‐497‐5p, miR‐129‐5p, miR‐5590‐3p, miR‐873‐5p, among others) to upregulate downstream targets such as CDCA7, FGFRL1, USP21, WEE1, PD‐L1, SEPT2, MCL1, HNRNPK, KIAA1522, and GTPBP4. These interactions contribute not only to tumor growth and metastasis but also to therapeutic resistance in multiple settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Outside the realm of oncology, FGD5‐AS1 plays important roles in inflammatory and ischemic conditions. In periodontitis and sepsis, for example, upregulation of FGD5‐AS1 mitigates inflammatory injury by modulating microRNA axes such as miR‐142‐3p/SOCS6 and miR‐133a‐3p/AQP1, respectively, thereby restraining NF‐κB signaling and reducing pro‐inflammatory cytokine release."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": " In cardiomyocytes subjected to hypoxic or oxygen–glucose deprivation injury, FGD5‐AS1 expression is reduced; its ectopic expression alleviates oxidative stress and apoptosis via regulation of miR‐195/RORA and miR‐106a/b‐mediated pathways, underscoring its cardioprotective potential."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Moreover, in osteoarthritis models, FGD5‐AS1 has been shown to preserve chondrocyte viability and extracellular matrix integrity by modulating the miR‐302d‐3p/TGFBR2 axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Additional evidence indicates that FGD5‐AS1 may also influence tumor stemness, serve as a prognostic biomarker in malignancies such as melanoma, and confer drug resistance in cisplatin‐treated tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "17"}]}, {"type": "t", "text": " Moreover, its role in intercellular communication via exosomes suggests that FGD5‐AS1 released from tumor cells can impact the tumor microenvironment by promoting angiogenesis and vascular permeability through targeting endothelial miR‐6838‐5p/VAV2."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, FGD5‐AS1 functions as a critical regulatory molecule by acting as a ceRNA that modulates key signaling pathways in diverse cellular contexts. Its dysregulation contributes to tumor progression, chemoresistance, and inflammatory as well as ischemic injuries. Thus, FGD5‐AS1 represents both a promising prognostic biomarker and a potential therapeutic target in a broad spectrum of diseases"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "–."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ding Li, Xiaohui Jiang, Xueliang Zhang, et al. 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