{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nCYTOR, also known as LINC00152, is a long non‐coding RNA that is frequently overexpressed in a broad spectrum of human cancers—including gastric, colorectal, hepatocellular carcinoma, lung, and others—and its aberrant expression is strongly associated with advanced tumor stage, aggressive invasion, metastasis, and poor clinical outcome. Elevated CYTOR levels have been reported in patient tissues and even detected in circulating biological fluids, underscoring its potential as both a diagnostic and prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, CYTOR exerts its oncogenic functions via multiple interrelated pathways. It can act as a competing endogenous RNA (ceRNA) by sponging a variety of microRNAs—for example, miR‐193a‐3p, miR‐125a‑5p, miR‐125b, miR‐103, miR‐215, and others—in turn derepressing downstream effectors such as ERBB4, serum response factor (SRF), MCL‑1, FYN, MACC1, CDK14, LASP1, and PIK3CA. In addition, CYTOR directly interacts with proteins like β‑catenin and heterogeneous nuclear ribonucleoproteins (e.g. HNRNPC) to promote epithelial–mesenchymal transition (EMT), enhance cell cycle progression, and confer chemoresistance. Its transcription is driven by oncogenic transcription factors including FOXD1, TCF3, FOXM1, YY1, and STAT3, thereby linking CYTOR to key signaling cascades such as the PI3K/AKT, mTOR, Hippo, MAPK, and Wnt/β‑catenin pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBecause of its central role in tumor progression—including promotion of proliferation, invasion, EMT and chemoresistance—CYTOR is emerging as a promising therapeutic target. Preclinical strategies that suppress CYTOR (for example, using small interfering RNAs delivered via nanoparticle formulations) have successfully inhibited tumor growth and metastatic spread in various cancer models. 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