{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LINC01140 is a long intergenic non‐coding RNA that has emerged as a multifunctional regulator in both cancer and inflammatory disorders. In muscle‐invasive bladder cancer, LINC01140 is upregulated and promotes cell viability, migration, invasion, and macrophage M2 polarization via a competing endogenous RNA (ceRNA) network involving miR‑140‑5p and FGF9."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In sarcoma, however, lower LINC01140 expression is observed in metastatic tumors, with reduced levels correlating with a poorer prognosis; mechanistic analyses suggest its involvement in pathways such as the epithelial–mesenchymal transition and modulation of immune responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " In non–small cell lung cancer, LINC01140 acts as a tumor suppressor by sponging miR‑4742‑5p to favor TACC1 expression, thereby reducing invasion, diminishing cisplatin resistance, and triggering apoptosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In breast cancer, circulating LINC01140 is found to be downregulated, and higher expression in tumors is associated with earlier disease stages and longer relapse‐free survival, indicating its potential as a diagnostic biomarker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond cancer cell–intrinsic effects, LINC01140 participates in the regulation of inflammatory responses. In macrophages stimulated by oxidized low‐density lipoprotein, LINC01140 exerts an anti‐inflammatory role by negatively regulating miR‑23b and subsequently promoting A20 expression to suppress NF‑κB activity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " Similarly, in lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF), LINC01140 is upregulated and supports cellular proliferation while dampening inflammatory cytokine production, indicating its involvement in tissue homeostasis and fibrosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In other tumor types, LINC01140 displays additional context‐dependent roles. In lung cancer, for example, LINC01140 is overexpressed and promotes proliferation, migration, invasion, and even immune escape by interacting with miR‑33a‑5p/miR‑33b‑5p—thereby protecting c‑Myc and facilitating PD‑L1 upregulation—contributing to tumor growth and metastasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": " In glioma, upregulation of LINC01140 drives tumor progression by repressing miR‑199a‑3p and enhancing ZHX1 expression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": " Furthermore, LINC01140 has been incorporated into prognostic lncRNA signatures in gastric cancer and has been identified as a hub within ceRNA networks in endometriosis, underscoring its diverse biological relevance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these studies reveal that LINC01140 plays multifaceted and context‐dependent roles. It can function either as an oncogenic factor or as a tumor‐suppressive and anti‐inflammatory molecule by modulating ceRNA networks and regulating key downstream targets. Such versatility not only impacts cancer cell aggressiveness, chemoresistance, and immune escape but also influences inflammatory signaling and tissue remodeling, highlighting LINC01140’s potential as a prognostic biomarker and therapeutic target across a range of malignancies and inflammatory disorders.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Shuiqing Wu, Ran Xu, Xuan Zhu, et al. 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