{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LINC00152, also known as CYTOR, is frequently overexpressed in diverse cancers—including gastric, colon, hepatocellular, non‐small cell lung, and triple‐negative breast cancers—and its elevated expression correlates with aggressive clinicopathological features such as larger tumor size, deeper invasion, enhanced metastasis, and poorer overall survival."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Mechanistically, LINC00152 appears to promote oncogenesis through multiple pathways. In gastric and lung cancers, it interacts with epigenetic regulators such as EZH2 to repress tumor suppressor genes—including p15, p21, and IL24—thereby stimulating cell cycle progression and proliferation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}, {"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In colon cancer and triple‐negative breast cancer, LINC00152 functions as a competing endogenous RNA to sponge microRNAs (for example, miR‑193a‑3p), which results in the de‐repression of targets such as ERBB4 and ETS1; these events lead to activation of downstream signaling cascades including the PI3K/AKT and mTOR pathways and confer chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "10"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition, direct binding of LINC00152 to proteins such as EGFR has been shown to further activate the PI3K/AKT signaling cascade in gastric and lung cancers"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}, {"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", while its critical role in cell cycle regulation is underscored by findings that depletion of LINC00152 leads to arrest during mitosis, particularly in prometaphase."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, in hepatocellular carcinoma LINC00152 has been implicated in the activation of the mTOR pathway and the promotion of cell cycle progression via upregulation of CCND1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", while its involvement as a serum biomarker in gastric cancer further supports its potential clinical utility."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings demonstrate that LINC00152 acts as a multifaceted oncogene by modulating key signaling and epigenetic mechanisms that drive tumor proliferation, invasion, metastasis, and chemoresistance. The diverse functional roles of LINC00152 underscore its value as a promising diagnostic biomarker and therapeutic target across multiple cancer types.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Qianqian Pang, Jiaxin Ge, Yongfu Shao, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Increased expression of long intergenic non-coding RNA LINC00152 in gastric cancer and its clinical significance."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Tumour Biol (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s13277-014-1709-3"}], "href": "https://doi.org/10.1007/s13277-014-1709-3"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24523021"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24523021"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Tian Yang, Hongmei Zeng, Wanqing Chen, et al. 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