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The N-Myc-Responsive LncRNA MILIP Promotes Non-Homologous DNA End Joining to Alleviate Genotoxic Stress in Human Neuroblastoma

ABSTRACT: lncRNAMILIP promotes the NHEJ pathway through facilitating Ku70-Ku80 heterodimerization and is involved in the resistance to DNA-damaging therapeutics in neuroblastoma cells.

ORGANISM(S): Homo Sapiens

SUBMITTER: Xudong Zhang

PROVIDER: PXD033372 | iProX | Fri Apr 22 00:00:00 BST 2022

REPOSITORIES: iProX

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The N-Myc-responsive lncRNA MILIP promotes DNA double-strand break repair through non-homologous end joining.

Wang Pei Lin PL Teng Liu L Feng Yu Chen YC Yue Yi Meng YM Han Man Man MM Yan Qianqian Q Ye Kaihong K Tang Cai Xia CX Zhang Sheng Nan SN Fei Qi Teng T Zhao Xiao Hong XH La Ting T Zhang Yuan Yuan YY Li Jin Ming JM Hu Bin B Xu Dengfei D Cang Shundong S Wang Li L Jin Lei L Thorne Rick F RF Zhang Yuwei Y Liu Tao T Zhang Xu Dong XD

Proceedings of the National Academy of Sciences of the United States of America 20221129 49

The protooncoprotein N-Myc, which is overexpressed in approximately 25% of neuroblastomas as the consequence of <i>MYCN</i> gene amplification, has long been postulated to regulate DNA double-strand break (DSB) repair in neuroblastoma cells, but experimental evidence of this function is presently scant. Here, we show that N-Myc transcriptionally activates the long noncoding RNA MILIP to promote nonhomologous end-joining (NHEJ) DNA repair through facilitating Ku70-Ku80 heterodimerization in neuro ...[more]

PMID: 36445966

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