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Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis

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Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis. / Pauzaite, Tekle; Thacker, Urvi; Tollitt, James et al.
In: Biomolecules, Vol. 7, No. 1, 2017.

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Pauzaite T, Thacker U, Tollitt J, Copeland NA. Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis. Biomolecules. 2017;7(1). Epub 2016 Dec 27. doi: 10.3390/biom7010001

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@article{b234c4179ac44c30991d3fb8b5364bde,
title = "Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis",
abstract = "Precise duplication of the genome is a prerequisite for the health and longevity of multicellular organisms. The temporal regulation of origin specification, replication licensing, and firing at replication origins is mediated by the cyclin-dependent kinases. Here the role of Cip1 interacting Zinc finger protein 1 (Ciz1) in regulation of cell cycle progression is discussed. Ciz1 contributes to regulation of the G1/S transition in mammalian cells. Ciz1 contacts the pre-replication complex (pre-RC) through cell division cycle 6 (Cdc6) interactions and aids localization of cyclin A- cyclin-dependent kinase 2 (CDK2) activity to chromatin and the nuclear matrix during initiation of DNA replication. We discuss evidence that Ciz1 serves as a kinase sensor that regulates both initiation of DNA replication and prevention of re-replication. Finally, the emerging role for Ciz1 in cancer biology is discussed. Ciz1 is overexpressed in common tumors and tumor growth is dependent on Ciz1 expression, suggesting that Ciz1 is a driver of tumor growth. We present evidence that Ciz1 may contribute to deregulation of the cell cycle due to its ability to alter the CDK activity thresholds that are permissive for initiation of DNA replication. We propose that Ciz1 may contribute to oncogenesis by induction of DNA replication stress and that Ciz1 may be a multifaceted target in cancer therapy.",
keywords = "genome stability, CDK, DNA replication stress, Cell cycle, cancer, Ciz1",
author = "Tekle Pauzaite and Urvi Thacker and James Tollitt and Copeland, {Nikki A.}",
year = "2017",
doi = "10.3390/biom7010001",
language = "English",
volume = "7",
journal = "Biomolecules",
issn = "2218-273X",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "1",

}

RIS

TY - JOUR

T1 - Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis

AU - Pauzaite, Tekle

AU - Thacker, Urvi

AU - Tollitt, James

AU - Copeland, Nikki A.

PY - 2017

Y1 - 2017

N2 - Precise duplication of the genome is a prerequisite for the health and longevity of multicellular organisms. The temporal regulation of origin specification, replication licensing, and firing at replication origins is mediated by the cyclin-dependent kinases. Here the role of Cip1 interacting Zinc finger protein 1 (Ciz1) in regulation of cell cycle progression is discussed. Ciz1 contributes to regulation of the G1/S transition in mammalian cells. Ciz1 contacts the pre-replication complex (pre-RC) through cell division cycle 6 (Cdc6) interactions and aids localization of cyclin A- cyclin-dependent kinase 2 (CDK2) activity to chromatin and the nuclear matrix during initiation of DNA replication. We discuss evidence that Ciz1 serves as a kinase sensor that regulates both initiation of DNA replication and prevention of re-replication. Finally, the emerging role for Ciz1 in cancer biology is discussed. Ciz1 is overexpressed in common tumors and tumor growth is dependent on Ciz1 expression, suggesting that Ciz1 is a driver of tumor growth. We present evidence that Ciz1 may contribute to deregulation of the cell cycle due to its ability to alter the CDK activity thresholds that are permissive for initiation of DNA replication. We propose that Ciz1 may contribute to oncogenesis by induction of DNA replication stress and that Ciz1 may be a multifaceted target in cancer therapy.

AB - Precise duplication of the genome is a prerequisite for the health and longevity of multicellular organisms. The temporal regulation of origin specification, replication licensing, and firing at replication origins is mediated by the cyclin-dependent kinases. Here the role of Cip1 interacting Zinc finger protein 1 (Ciz1) in regulation of cell cycle progression is discussed. Ciz1 contributes to regulation of the G1/S transition in mammalian cells. Ciz1 contacts the pre-replication complex (pre-RC) through cell division cycle 6 (Cdc6) interactions and aids localization of cyclin A- cyclin-dependent kinase 2 (CDK2) activity to chromatin and the nuclear matrix during initiation of DNA replication. We discuss evidence that Ciz1 serves as a kinase sensor that regulates both initiation of DNA replication and prevention of re-replication. Finally, the emerging role for Ciz1 in cancer biology is discussed. Ciz1 is overexpressed in common tumors and tumor growth is dependent on Ciz1 expression, suggesting that Ciz1 is a driver of tumor growth. We present evidence that Ciz1 may contribute to deregulation of the cell cycle due to its ability to alter the CDK activity thresholds that are permissive for initiation of DNA replication. We propose that Ciz1 may contribute to oncogenesis by induction of DNA replication stress and that Ciz1 may be a multifaceted target in cancer therapy.

KW - genome stability

KW - CDK

KW - DNA replication stress

KW - Cell cycle

KW - cancer

KW - Ciz1

U2 - 10.3390/biom7010001

DO - 10.3390/biom7010001

M3 - Journal article

C2 - 28036012

VL - 7

JO - Biomolecules

JF - Biomolecules

SN - 2218-273X

IS - 1

ER -