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The tumor-associated YB-1 protein: new player in the circadian control of cell proliferation

Pagano, Cristina 1; Martino, Orsola di; Ruggiero, Gennaro 1; Maria Guarino, Andrea; Mueller, Nathalie 1; Siauciunaite, Rima 1; Reischl, Markus ORCID iD icon 2; Simon Foulkes, Nicholas; Vallone, Daniela 1; Calabro, Viola
1 Institut für Toxikologie und Genetik (ITG), Karlsruher Institut für Technologie (KIT)
2 Institut für Angewandte Informatik (IAI), Karlsruher Institut für Technologie (KIT)

Abstract:

Correct spatial and temporal control of cell proliferation is of fundamental importance for tissue homeostasis. Its deregulation has been associated with several pathological conditions. In common with almost every aspect of plant and animal biology, cell proliferation is dominated by day-night rhythms generated by the circadian clock. However, our understanding of the crosstalk between the core clock and cell cycle control mechanisms remains incomplete. In this study, using zebrafish as a vertebrate model system, we show that the nuclear localization of the Y-box binding protein 1 (YB-1), a regulator of cyclin expression and a hallmark of certain cancers, is robustly regulated by the circadian clock. We implicate clock-controlled changes in YB-1 SUMOylation as one of the mechanisms regulating its periodic nuclear entry at the beginning of the light phase. Furthermore, we demonstrate that YB-1 nuclear protein is able to downregulate cyclin A2 mRNA expression in zebrafish via its direct interaction with the cyclin A2 promoter. Thus, by acting as a direct target of cyclic posttranslational regulatory mechanisms, YB-1 serves as one bridge between the circadian clock and its cell cycle control.


Verlagsausgabe §
DOI: 10.5445/IR/1000064916
Veröffentlicht am 12.02.2018
Originalveröffentlichung
DOI: 10.18632/oncotarget.14051
Scopus
Zitationen: 17
Web of Science
Zitationen: 17
Dimensions
Zitationen: 19
Cover der Publikation
Zugehörige Institution(en) am KIT Institut für Angewandte Informatik (IAI)
Institut für Toxikologie und Genetik (ITG)
Publikationstyp Zeitschriftenaufsatz
Publikationsjahr 2017
Sprache Englisch
Identifikator ISSN: 1949-2553
urn:nbn:de:swb:90-649163
KITopen-ID: 1000064916
HGF-Programm 47.01.01 (POF III, LK 01) Biol.Netzwerke u.Synth.Regulat. ITG+ITC
Erschienen in OncoTarget
Verlag Impact Journals
Band 8
Heft 4
Seiten 6193-6205
Bemerkung zur Veröffentlichung Gefördert durch den KIT-Publikationsfonds
Vorab online veröffentlicht am 20.12.2016
Nachgewiesen in Dimensions
Scopus
Web of Science
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