{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long intergenic non‐coding RNA LINC01123 has emerged as a critical oncogenic regulator across a broad spectrum of human malignancies and even non‐malignant vascular disorders. Elevated LINC01123 expression is documented in lung cancers—including non‐small cell lung cancer where it is upregulated via c‐Myc and promotes both proliferation and aerobic glycolysis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "and lung adenocarcinoma, where it accelerates malignant progression through a ceRNA network involving miR-449b-5p and NOTCH1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "(also contributing to cisplatin resistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In osteosarcoma, LINC01123 functions as a competing endogenous RNA (ceRNA) for miR-516b-5p to de-repress Gli1 expression, thereby enhancing proliferation and metastasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Similarly, in head and neck squamous cell carcinoma (HNSCC) its ceRNA activity—sponging miR-214-3p to regulate targets such as B7-H3—and its prognostic impact have been reported."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " In colon and colorectal cancers, LINC01123 promotes cell proliferation, migration, invasion, angiogenesis, and chemoresistance by modulating miR-34c-5p and interacting with key effectors such as VEGFA and SRSF7."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Beyond its oncogenic roles, increased LINC01123 in oxidized LDL-treated vascular smooth muscle cells facilitates proliferation and migration via the miR-1277-5p/KLF5 axis, suggesting a role in fibrous plaque formation in carotid atherosclerosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": " In glioma, LINC01123 contributes to radioresistance by sponging miR-151a and upregulating CENPB"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", while in oral squamous cell carcinoma its interaction with miR-34a-5p enhances proliferation, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " In endometrial cancer, transcriptional activation by STAT1 leads to LINC01123 overexpression that, by sponging miR-516b to regulate KIF4A, drives tumor growth, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Hepatocellular carcinoma studies further underscore its association with poor clinical features through promotion of proliferation, migration, and invasion"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", and in triple-negative breast cancer, FOXC1-induced LINC01123 modulates the miR-663a/CMIP axis to regulate proliferation and apoptosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " Finally, early evidence also implicates LINC01123 in cervical cancer progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings elucidate that LINC01123 exerts its oncogenic functions primarily through acting as a ceRNA that sequesters multiple tumor-suppressive microRNAs. This sponging activity leads to the de-repression of a variety of downstream oncogenic targets—including c-Myc, NOTCH1, Gli1, VEGFA, KLF5, CENPB, and CMIP—and the subsequent activation of pathways related to cell proliferation, epithelial–mesenchymal transition, chemoresistance, and even immune escape. The transcriptional upregulation of LINC01123 by factors such as c-Myc, ZEB1, FOXC1, and STAT1 further integrates it into key oncogenic regulatory networks, making it a promising prognostic biomarker and therapeutic target across multiple cancer types as well as in related vascular pathologies."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}, {"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "7"}, {"type": "fg_fs", "start_ref": "9", "end_ref": "11"}, {"type": "fg_f", "ref": "8"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_f", "ref": "13"}, {"type": "fg_f", "ref": "6"}, {"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Qian Hua, Mingming Jin, Baoming Mi, et al. 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