{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LINC00052 is a long non‐coding RNA with multifaceted, context‐dependent functions that have been implicated in both tumor suppression and tumor promotion as well as in non‐malignant conditions. In certain cancers such as hepatocellular carcinoma, colorectal cancer, glioma, and pancreatic cancer, LINC00052 is expressed at low levels, and its overexpression suppresses cell proliferation, migration, invasion, and metastasis by acting as a competing endogenous RNA that sponges specific microRNAs—in turn downregulating oncogenic targets like NTRK3, SOX9, CALCOCO1, and IGF2."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": " In contrast, in specific subtypes of breast cancer and in gastric cancer, high LINC00052 expression promotes tumorigenesis by correlating with enhanced receptor‐mediated oncogenic signaling (for example, HER3 signaling) and by facilitating activation of the Wnt/β‐catenin pathway through β‐catenin methylation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond oncology, LINC00052 also regulates key processes in non‐cancer pathologies. For instance, in neuropathic pain models, its elevated expression promotes neuroinflammation via a microRNA‐dependent mechanism that modulates JAK1 levels"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", and in acute kidney injury models, altered LINC00052 expression affects hypoxia‐induced cell proliferation, apoptosis, and inflammatory cytokine production."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, studies in breast cancer spheroids have implicated LINC00052 in the modulation of cholesterol metabolic pathways and cellular motility"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", and its inclusion in diagnostic panels for triple‐negative breast cancer and tongue squamous cell carcinoma underscores its potential utility as a prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " A recent review further emphasizes the diverse roles of LINC00052 in tumorigenesis across multiple cancer types"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", while additional evidence suggests that LINC00052 may also impact oncogenic signaling via cytoskeletal remodeling and the Notch/β‐catenin/NF‐κB axis in breast cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings indicate that LINC00052 functions as a versatile regulator, acting either as a tumor suppressor or promoter depending on the cellular context, and highlight its promise as both a diagnostic biomarker and a potential therapeutic target.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Dongmei Xiong, Yanrui Sheng, Shijia Ding, et al. 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