{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LINC01116 is a long non‐coding RNA that is consistently found to be overexpressed in a wide range of human malignancies and even in non‐malignant pathological conditions, where it predominantly functions as an oncogene. In glioma, for example, LINC01116 enhances cell proliferation, migration, invasion, and angiogenesis by acting as a competing endogenous RNA (ceRNA) that sponges microRNA‐31–5p to derepress VEGFA expression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": " In colorectal cancer, LINC01116 promotes tumor progression and angiogenesis by recruiting EZH2 to silence tumor‐suppressive genes such as TPM1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ", while in bladder cancer it modulates the expression of ELK3 and HOXD8, establishing a positive feedback loop that favors disease progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In osteosarcoma, LINC01116 binds to EZH2 and suppresses key tumor suppressors such as PTEN and p53, thereby facilitating cell cycle progression and invasion; it can also upregulate IL6R via sponging miR‐520a–3p to activate the JAK–STAT pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " In endometriosis, it contributes to the proliferation and migration of ectopic endometrial stromal cells through regulating the miR‐9–5p/FOXP1 axis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", and in nasopharyngeal carcinoma LINC01116 enhances MYC translation via direct interaction with its mRNA, thus establishing a positive feedback loop that drives tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n LINC01116 is also implicated in other cancers. In head and neck squamous cell carcinoma and gastric cancer, its upregulation is correlated with advanced clinical stage and enhanced epithelial–mesenchymal transition (EMT), leading to increased cell migration and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " In pituitary adenoma, it functions as a ceRNA for miR‐744–5p to upregulate HOXB8, thereby promoting proliferation, migration, and EMT"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ", and in lung adenocarcinoma, LINC01116 has been linked not only to aggressive tumor behavior via an AKT‐dependent mechanism"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "but also to the development of cisplatin resistance through modulation of EMT."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Additional studies have revealed that LINC01116 exerts its oncogenic influence by sponging various microRNAs—including miR‐203 in keloid formation"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ", miR‐93–5p in small cell lung cancer to upregulate STAT3"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": ", and miR‐744–5p in both nasopharyngeal carcinoma and prostate cancer to regulate targets such as MYC, HOXB8, and UBE2L3."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "21"}]}, {"type": "t", "text": " In non‐small cell lung cancer, it has been linked to resistance to EGFR tyrosine kinase inhibitors by altering IFI44 expression"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": ", and in oral squamous cell carcinoma, it promotes EMT and metastasis by sponging miR‐136 to regulate FN1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond its mechanistic roles, LINC01116 is frequently incorporated into multi‐lncRNA prognostic signatures for diverse cancers—including hepatocellular carcinoma, lung adenocarcinoma, and breast cancer—underscoring its value as an independent risk factor and potential biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "28"}]}, {"type": "t", "text": " Collectively, through its function as a molecular sponge for multiple microRNAs (including miR‐31–5p, miR‐744–5p, miR‐9–5p, miR‐520a–3p, and miR‐3141), LINC01116 dysregulates key oncogenic and tumor‐suppressive pathways—affecting targets such as VEGFA, FOXP1, MYC, STAT3, HOXB8, CDCA4, IL6R, TGF‐β1, and FN1—which ultimately promotes tumor cell proliferation, invasion, migration, EMT, and resistance to therapy. These multifaceted interactions make LINC01116 a promising target for diagnostic and therapeutic strategies across a broad spectrum of diseases.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jingliang Ye, Junle Zhu, Huairui Chen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A novel lncRNA-LINC01116 regulates tumorigenesis of glioma by targeting VEGFA."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Cancer (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/ijc.32483"}], "href": "https://doi.org/10.1002/ijc.32483"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31144303"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31144303"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Teng Wang, Lihua Cao, Xin Dong, et al. 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