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. 2016 Dec 27;7(1):1. doi: 10.3390/biom7010001

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© 2016 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Ciz1 may contribute to DNA replication stress via stimulation of oncogenic transcription and deregulation of the cell cycle. (A) Oncogenic transcriptional activation mediated by Ciz1 is shown. In this example, estrogen receptor (ER) is sensitized by Ciz1 interactions leading to a positive feedback mechanism, increasing Ciz1 transcript levels. Ciz1 also increases oncogenic transcription with Yes associated protein 1/ Tafazzin (YAP/TAZ) and Beta catenin/Wnt (Int/Wingless) signaling [77,79,80]; (B) Ciz1 can greatly enhance the permissive concentration of cyclin A-CDK2 that can facilitate initiation of DNA replication. In this model, deregulation of cyclin expression associated with oncogenic activation increases CDK activity. Increased Ciz1 protein may enable adaption of cells to this high CDK environment and continued DNA replication at wider concentrations of cyclin-dependent kinase activity. Both mechanisms induce DNA replication stress that underpins the early events in tumorigenesis.