{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long intergenic non‐protein coding RNA 205 (LINC00205) is emerging as an important oncogenic long non‐coding RNA whose overexpression has been reported in multiple tumor types, including hepatocellular carcinoma (HCC), lung cancer, hepatoblastoma, gastric cancer, and pancreatic ductal adenocarcinoma. In several studies on HCC, LINC00205 has been shown to promote tumorigenic behaviors by acting as a competing endogenous RNA (ceRNA) that sequesters tumor‐suppressive microRNAs. For instance, LINC00205 directly binds to miR‑122‑5p, thereby promoting proliferation, migration, and invasion of HCC cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In another HCC study, it sponges miR‑26a‑5p to upregulate CDK6 expression and facilitate cell cycle progression, with its transcription activated by the factor YY1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " Moreover, LINC00205 modulates HCC progression by binding miR‑184, which in turn positively regulates EPHX1 levels, thus influencing proliferation and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In lung cancer, LINC00205 has been implicated in malignant progression through distinct mechanisms. One study demonstrated that it recruits the RNA‐binding protein FUS to stabilize CSDE1 mRNA, thereby enhancing CSDE1 expression and promoting proliferation and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Complementary findings in lung adenocarcinoma revealed that LINC00205 contributes to enhanced cell proliferation and migration by sponging miR‑185‑5p."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Additional evidence from studies on hepatoblastoma and gastric cancer further underscores its oncogenic role. In hepatoblastoma, LINC00205 promotes tumor growth by binding to miR‑154‑3p, which releases its target, ROCK1, thus activating the MAPK signaling pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " In gastric cancer, LINC00205 acts as a ceRNA for miR‑26a, leading to the deregulation of downstream genes such as HMGA2, EZH2, and USP15 that are essential for cell survival and epithelial‐mesenchymal transition."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond its direct roles in promoting invasion, proliferation, and metastasis across these malignancies, elevated LINC00205 expression has been associated with poor prognosis and may serve as a valuable biomarker for tumor recurrence and patient survival in both HCC and pancreatic cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these studies reveal that LINC00205 functions primarily as an oncogenic ceRNA that interacts with distinct microRNAs or RNA‐binding proteins to regulate critical downstream target genes and signaling pathways involved in cancer cell proliferation, migration, invasion, and apoptosis. Its multi‐modal mechanism of action highlights its potential as both a prognostic biomarker and a therapeutic target in several malignancies.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lei Zhang, Yun Wang, Jingjing Sun, et al. "}, {"type": "b", "children": [{"type": "t", "text": "LINC00205 promotes proliferation, migration and invasion of HCC cells by targeting miR-122-5p."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Pathol Res Pract (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.prp.2019.152515"}], "href": "https://doi.org/10.1016/j.prp.2019.152515"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31272761"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31272761"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "T Cheng, Y Yao, S Zhang, et al. 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