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LINP1 (Long non-coding RNA in non-homologous end joining pathway 1) is a long non-coding RNA that acts as a molecular scaffold for the assembly of the non-homologous end joining (NHEJ) DNA repair machinery—specifically interacting with Ku70–Ku80 and DNA-PKcs to promote repair of DNA double-strand breaks. LINP1 is overexpressed in several cancers, notably triple-negative breast cancer and esophageal squamous cell carcinoma, and regulates cell proliferation, metastasis, EMT, and resistance to chemotherapeutic drugs such as doxorubicin and 5-fluorouracil. Knockdown of LINP1 leads to cell cycle arrest, apoptosis, and decreased tumorigenic potential, identifying it as both a potential therapeutic target and a prognostic biomarker in cancer. LINP1’s activity also links it to chemoresistance, suggesting a role in modulating sensitivity to DNA-damaging treatments in oncology.
Drug-induced apoptosis (e.g., doxorubicin) is inhibited by LINP1 overexpression, which promotes NHEJ DNA repair and reduces DNA damage-mediated cell death.
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