{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe study reveals that the long noncoding RNA MILIP functions as a critical mediator of DNA repair in neuroblastoma cells. Specifically, MILIP is transcriptionally activated by the proto‐oncogene N‐Myc, and its elevated expression correlates with adverse clinical outcomes. Once induced, MILIP promotes nonhomologous end‐joining (NHEJ) by binding to both Ku70 and Ku80, thereby facilitating their heterodimerization—a crucial step for efficient repair of double‐strand DNA breaks. As a consequence, knockdown of MILIP leads to the accumulation of unrepaired DNA damage, induces apoptosis, and impairs tumor cell viability, while also sensitizing neuroblastoma cells to DNA‐damaging agents such as cisplatin. These findings underscore MILIP’s role as an indispensable N‐Myc downstream effector in maintaining DNA integrity and promoting tumor survival, highlighting its potential as a therapeutic target for neuroblastoma treatment."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Pei Lin Wang, Liu Teng, Yu Chen Feng, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The N-Myc-responsive lncRNA MILIP promotes DNA double-strand break repair through non-homologous end joining."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Proc Natl Acad Sci U S A (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1073/pnas.2208904119"}], "href": "https://doi.org/10.1073/pnas.2208904119"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "36445966"}], "href": "https://pubmed.ncbi.nlm.nih.gov/36445966"}]}]}]}