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

Title
Mutual regulation between DNA-PKcs and snail1 leads to increased genomic instability and aggressive tumor characteristics
Authors
Pyun B.-J.Seo H.R.Lee H.-J.Jin Y.B.Kim E.-J.Kim N.H.Kim H.S.Nam H.W.Yook J.I.Lee Y.S.
Ewha Authors
이윤실
SCOPUS Author ID
이윤실scopus
Issue Date
2013
Journal Title
Cell Death and Disease
ISSN
2041-4889JCR Link
Citation
vol. 4, no. 2
Indexed
SCIE; SCOPUS WOS scopus
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 DNAPKcs, 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. © 2013 Macmillan Publishers Limited All rights reserved.
DOI
10.1038/cddis.2013.43
Appears in Collections:
약학대학 > 약학과 > Journal papers
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