{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n FOXD2‐AS1 is a long noncoding RNA that is aberrantly upregulated in a wide variety of human cancers and other pathologic conditions, and its dysregulation is strongly correlated with aggressive clinical features and poor patient prognosis (38,41). In multiple solid tumors—including gastric, colorectal, bladder, non‐small cell lung, hepatocellular, breast, nasopharyngeal, esophageal, glioma, cholangiocarcinoma, gallbladder, cervical, tongue squamous cell, pancreatic, and cutaneous melanoma cancers—FOXD2‐AS1 exerts an oncogenic function by promoting cell proliferation, migration, invasion, epithelial–mesenchymal transition (EMT), and stemness, as well as by fostering chemoresistance (1–6, 8, 10–14, 16, 17, 19, 22, 27, 29, 31, 36, 39, 40).\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Mechanistically, FOXD2‐AS1 predominantly functions as a competing endogenous RNA, sequestering multiple microRNAs (such as miR‑206, miR‑185‐5p, miR‑143, miR‑31, miR‑27a‑3p, miR‑150‑5p, miR‑98‑5p, miR‑760, miR‑30a‑3p, and miR‑331‑3p) to indirectly upregulate target oncogenes including EphB3, cell division regulators (e.g. CCND2 and CDK1), ABCC3, PFN2, MAP3K1, COX‑2, and E2F3 (1, 3–5, 11, 12, 14, 16, 17, 23, 27, 29, 31, 37, 39). In addition, FOXD2‐AS1 interacts with key epigenetic regulators such as EZH2 and LSD1 and with DNA methylation or transcription factors (for example, CREB1, TAF‑1, and DNMT1) to repress tumor suppressor genes including DKK1, p21, CDKN1B, MLH1, and CDX1 (4, 15, 20, 21, 32, 33). Consequently, activation of several signaling pathways—including Wnt/β‑catenin, PI3K/AKT, Hippo/YAP, Notch, NF‑κB, and ERK/MAPK—has been observed upon FOXD2‑AS1 upregulation, thereby further enhancing tumor progression (6, 9, 16, 17, 19, 24, 27, 31, 34, 36).\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond cancer, increased FOXD2‐AS1 levels have been implicated in non‐malignant diseases such as osteoarthritis and rheumatoid arthritis. In osteoarthritis, FOXD2‐AS1 promotes chondrocyte viability, inflammation, and extracellular matrix degradation through modulation of the miR‑206/Cyclin D1 axis and the miR‑27a‑3p/TLR4 pathway (7, 9), while in rheumatoid arthritis it enhances fibroblast‑like synoviocyte proliferation and invasion via a miR‑331‑3p/PIAS3 regulatory mechanism (26).\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, the studies indicate that FOXD2‑AS1 is a multifaceted oncogenic lncRNA whose upregulation not only drives tumorigenesis and progression via diverse molecular mechanisms but also represents a promising prognostic biomarker and potential therapeutic target across various cancers.\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n <!-- Hyperlinked citations -->\n <small>\n (1)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ", \n (2)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", \n (3)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ", \n (4)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", \n (5)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ", \n (6)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", \n (7)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ", \n (8)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", \n (9)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ", \n (10)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", \n (11)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": ", \n (12)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", \n (13)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", \n (14)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ", \n (15)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": ", \n (16)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ", \n (17)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ", \n (19)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": ", \n (20)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": ", \n (21)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": ", \n (22)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": ", \n (23)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": ", \n (24)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": ", \n (25)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": ", \n (26)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": ", \n (27)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": ", \n (28)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": ", \n (29)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": ", \n (30)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": ", \n (31)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "30"}]}, {"type": "t", "text": ", \n (32)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": ", \n (33)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": ", \n (34)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": ", \n (35)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "34"}]}, {"type": "t", "text": ", \n (36)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "35"}]}, {"type": "t", "text": ", \n (37)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": ", \n (38)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "37"}]}, {"type": "t", "text": ", \n (39)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "38"}]}, {"type": "t", "text": ", \n (40)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "39"}]}, {"type": "t", "text": ", \n (41)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "40"}]}, {"type": "t", "text": "</small>\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tong-Peng Xu, Wen-Yu Wang, Pei Ma, et al. 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