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Mutual regulation between DNA-PKcs and snail1 leads to increased genomic instability and aggressive tumor characteristics

Authors
 B-J Pyun  ;  H R Seo  ;  H-J Lee  ;  Y B Jin  ;  E-J Kim  ;  N H Kim  ;  H S Kim  ;  H W Nam  ;  J I Yook  ;  Y-S Lee 
Citation
 Cell Death & Disease, Vol.4 : 517-517, 2013 
Journal Title
 Cell Death & Disease 
ISSN
 2041-4889 
Issue Date
2013
Abstract
Although the roles of DNA-dependent protein kinase catalytic subunits (DNA-PKcs) in the non-homologous end joining (NHEJ) of DNA repair are well-recognized, the biological mechanisms and regulators by DNA-PKcs besides DNA repair, have not been clearly described. Here, we show that active DNA-PKcs caused by ionizing radiation, phosphorylated Snail1 at serine (Ser) 100, led to increased Snail1 stability. Furthermore, phosphorylated Snail1 at Ser100 reciprocally inhibited the kinase activity of DNA-PKcs, resulting in an inhibition of DNA repair activity. Moreover, Snail1 phosphorylation by DNA-PKcs was involved in genomic instability and aggressive tumor characteristics. Our results describe novel cellular mechanisms that affect genomic instability, sensitivity to DNA-damaging agents, and the migration of tumor cells by reciprocal regulation between DNA-PKcs and Snail1.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/86466
Files in This Item:
T201300528.pdf Download
DOI
10.1038/cddis.2013.43
Appears in Collections:
1. Journal Papers (연구논문) > 5. Research Institutes (연구소) > Oral Cancer Research Institute (구강종양연구소)
1. Journal Papers (연구논문) > 2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실)
Yonsei Authors
김남희(Kim, Nam Hee)
김현실(Kim, Hyun Sil)
육종인(Yook, Jong In)
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