{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nILF3-AS1, also referred to as ILF3 divergent transcript (ILF3-DT), is involved in diverse pathological processes through context‐dependent mechanisms. In melanoma, ILF3-AS1 is upregulated and contributes to aggressive tumor behavior by binding to the epigenetic regulator EZH2, which facilitates the suppression of the miR-200b/a/429 cluster. This repression leads to enhanced proliferation, migration, and invasion of melanoma cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " Similarly, in osteosarcoma, ILF3-AS1 is overexpressed—its expression being induced by the transcription factor SP1—and exerts an oncogenic role by modulating the miR-212/SOX5 axis, thereby promoting tumor progression and metastasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn neurological disorders such as temporal lobe epilepsy (TLE), ILF3-AS1 expression is significantly elevated. One study demonstrated that pro-inflammatory cytokines like interleukin-1β and TNF-α stimulate ILF3-AS1 expression in astrocytes, which in turn amplifies the production of inflammatory cytokines (e.g., IL-6 and TNF-α) and several matrix metalloproteinases while suppressing miR-212, thereby contributing to neuroinflammation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " A related investigation in TLE patients’ hippocampi further supports the involvement of ILF3-AS1 in mediating oxidative stress and inflammatory responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, in certain cancers ILF3-AS1 appears to have a tumor-suppressive function. In cervical cancer, ILF3-AS1 is downregulated compared with normal tissue; its overexpression inhibits cell proliferation and migration, promotes apoptosis, and suppresses epithelial–mesenchymal transition largely by counteracting miR-454-3p to restore PTEN expression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Additionally, preliminary work in nasopharyngeal carcinoma has identified a regulatory role for ILF3-AS1 in tumor biology, although the precise mechanisms remain to be fully clarified."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xiangjun Chen, Sha Liu, Xiaochun Zhao, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429 in melanoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biosci Rep (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1042/BSR20171031"}], "href": "https://doi.org/10.1042/BSR20171031"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28935763"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28935763"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Xiao-Hui Hu, Jian Dai, Hou-Lai Shang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "SP1-mediated upregulation of lncRNA ILF3-AS1 functions a ceRNA for miR-212 to contribute to osteosarcoma progression via modulation of SOX5."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.bbrc.2019.02.110"}], "href": "https://doi.org/10.1016/j.bbrc.2019.02.110"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30819403"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30819403"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Xiaodong Cai, Ling Long, Chao Zeng, et al. 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