| Literature DB >> 33564066 |
Ziyang Guo1,2, Yingchu Dai1, Wentao Hu1, Yongsheng Zhang3, Zhifei Cao3, Weiwei Pei1, Ningang Liu1, Jing Nie1, Anqing Wu1, Weidong Mao3, Lei Chang1, Bingyan Li1, Hailong Pei4, Tom K Hei5, Guangming Zhou6.
Abstract
Aneuploidy is a hallmark of genomic instability that leads to tumor initiation, progression, and metastasis. CDC20, Bub1, and Bub3 form the mitosis checkpoint complex (MCC) that binds the anaphase-promoting complex or cyclosome (APC/C), a crucial factor of the spindle assembly checkpoint (SAC), to ensure the bi-directional attachment and proper segregation of all sister chromosomes. However, just how MCC is regulated to ensure normal mitosis during cellular division remains unclear. In the present study, we demonstrated that LNC CRYBG3, an ionizing radiation-inducible long noncoding RNA, directly binds with Bub3 and interrupts its interaction with CDC20 to result in aneuploidy. The 261-317 (S3) residual of the LNC CRYBG3 sequence is critical for its interaction with Bub3 protein. Overexpression of LNC CRYBG3 leads to aneuploidy and promotes tumorigenesis and metastasis of lung cancer cells, implying that LNC CRYBG3 is a novel oncogene. These findings provide a novel mechanistic basis for the pathogenesis of NSCLC after exposure to ionizing radiation as well as a potential target for the diagnosis, treatment, and prognosis of an often fatal disease.Entities:
Year: 2021 PMID: 33564066 PMCID: PMC7946627 DOI: 10.1038/s41388-020-01601-8
Source DB: PubMed Journal: Oncogene ISSN: 0950-9232 Impact factor: 9.867