{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long stress‐induced non‐coding transcript 5 (LSINCT5) is a stress‐induced long non‐coding RNA that is frequently upregulated in a wide spectrum of human cancers—including breast, ovarian, gastrointestinal, bladder, non‐small cell lung, esophageal, osteosarcoma, and pancreatic cancers—and is also implicated in myocardial cell injury. Studies have demonstrated that elevated LSINCT5 expression promotes tumor cell proliferation, migration, invasion, and epithelial–mesenchymal transition, thereby contributing to tumor growth, metastasis, and poor patient prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": " In gastric and esophageal cancers, LSINCT5 is an element of diagnostic lncRNA panels and its high expression correlates with advanced clinical stage and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " In non‐small cell lung cancer, LSINCT5 promotes cell migration and viability by interacting with oncogenic factors – for instance, by binding to HMGA2 and inhibiting its proteasomal degradation – which subsequently leads to activation of the Wnt/β‐catenin signaling pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " Similarly, in bladder and oral squamous cell carcinomas, LSINCT5 exerts its pro‐tumorigenic effects via molecular sponging of specific microRNAs (such as miR‑185‑5p) and regulation of downstream targets involved in invasion and EMT."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Furthermore, in the context of myocardial injury, LSINCT5 mediates cardiomyocyte apoptosis by activating the caspase‑1/interleukin‑1β signaling cascade."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Finally, LSINCT5 has also been linked to drug resistance, as its high expression in lung cancer cells has been associated with erlotinib resistance likely via modulation of the Akt pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, LSINCT5 represents a multifunctional oncogenic lncRNA that acts through diverse mechanisms—including functioning as a competing endogenous RNA and physically interacting with key regulatory proteins—to activate oncogenic signaling pathways (such as Wnt/β‑catenin, PI3K/AKT, and p38MAPK), enhance tumor progression, and even modulate responses to chemotherapy. Its consistent overexpression across multiple tumor types and its association with adverse clinical features render LSINCT5 a promising candidate for novel diagnostic, prognostic, and therapeutic applications."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}, {"type": "fg_f", "ref": "6"}, {"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jessica M Silva, Nicole J Boczek, Michael W Berres, et al. "}, {"type": "b", "children": [{"type": "t", "text": "LSINCT5 is over expressed in breast and ovarian cancer and affects cellular proliferation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "RNA Biol (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.4161/rna.8.3.14800"}], "href": "https://doi.org/10.4161/rna.8.3.14800"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21532345"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21532345"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Mi-Die Xu, Peng Qi, Wei-Wei Weng, et al. 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