{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNKILA is a long non‐coding RNA that primarily exerts its function by directly interacting with the NF‑κB/IκB complex, thereby inhibiting IκBα phosphorylation and blocking p65 nuclear translocation. In several cancers—including breast, lung, tongue squamous cell, laryngeal, nasopharyngeal, esophageal, rectal, oral, cervical, and certain lymphomas as well as retinoblastoma—low NKILA expression is associated with enhanced NF‑κB activity, increased epithelial‐to‐mesenchymal transition, greater metastatic potential, and ultimately poorer clinical outcomes. In these settings, NKILA functions as a tumor suppressor by sensitizing tumor‐infiltrating lymphocytes to activation‐induced cell death, reducing cell proliferation, migration, and invasion, and even improving responses to radiotherapy and targeted therapy. Notably, however, context‐dependent exceptions have been observed: in cholangiocarcinoma and gliomas, NKILA may be upregulated and contribute to tumor progression by promoting the Warburg effect and angiogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in cancer, NKILA is a critical regulator of NF‑κB–mediated pathways in a range of non‐neoplastic conditions. It modulates inflammatory responses in vascular endothelial cells by affecting the expression of protective factors (for example, KLF4) and has been shown to suppress viral gene expression by inhibiting NF‑κB–driven transcription—thereby limiting replication of pathogens such as HIV‑1 and hepatitis B virus. NKILA also influences cellular responses in settings of inflammation, hypoxia, and oxidative stress, including sepsis‐induced acute kidney injury, osteoarthritis, myocardial and coronary artery diseases, and Mycoplasma pneumoniae–induced airway inflammation. Moreover, its role in regulating mRNA export via interaction with splicing regulators, as well as promoting osteogenic differentiation through RXFP1/PI3K–AKT signaling, underscores its multifunctional nature. NKILA’s participation in neurodegenerative processes, as observed in models of Alzheimer’s disease, and its altered expression in autoimmune conditions like ankylosing spondylitis and systemic lupus erythematosus further illustrate its diverse impact on cellular homeostasis and disease progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "31"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_fs", "start_ref": "32", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Di Huang, Jianing Chen, Linbin Yang, et al. 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