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Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors

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Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors. / Dalvai, M.; Mondesert, O.; Bourdon, J.-C.; Ducommun, B.; Dozier, C.

In: Oncogene, Vol. 30, No. 19, 2011, p. 2282-2288.

Research output: Contribution to journalArticle

Harvard

Dalvai, M, Mondesert, O, Bourdon, J-C, Ducommun, B & Dozier, C 2011, 'Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors' Oncogene, vol 30, no. 19, pp. 2282-2288., 10.1038/onc.2010.588

APA

Dalvai, M., Mondesert, O., Bourdon, J-C., Ducommun, B., & Dozier, C. (2011). Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors. Oncogene, 30(19), 2282-2288. 10.1038/onc.2010.588

Vancouver

Dalvai M, Mondesert O, Bourdon J-C, Ducommun B, Dozier C. Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors. Oncogene. 2011;30(19):2282-2288. Available from: 10.1038/onc.2010.588

Author

Dalvai, M.; Mondesert, O.; Bourdon, J.-C.; Ducommun, B.; Dozier, C. / Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors.

In: Oncogene, Vol. 30, No. 19, 2011, p. 2282-2288.

Research output: Contribution to journalArticle

Bibtex - Download

@article{8b57c4f883c34101b7eabb2a66e62e79,
title = "Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors",
keywords = "Cdc25B, p53, Sp1, NF-Y, CELL-CYCLE REGULATION, WILD-TYPE P53, BREAST-CANCER, DNA-DAMAGE, EXPRESSION, ACTIVATION, PHOSPHATASE, APOPTOSIS, GENES, TRIGGERS",
author = "M. Dalvai and O. Mondesert and J.-C. Bourdon and B. Ducommun and C. Dozier",
note = "MEDLINE® is the source for the MeSH terms of this document.",
year = "2011",
doi = "10.1038/onc.2010.588",
volume = "30",
number = "19",
pages = "2282--2288",
journal = "Oncogene",
issn = "0950-9232",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors

A1 - Dalvai,M.

A1 - Mondesert,O.

A1 - Bourdon,J.-C.

A1 - Ducommun,B.

A1 - Dozier,C.

AU - Dalvai,M.

AU - Mondesert,O.

AU - Bourdon,J.-C.

AU - Ducommun,B.

AU - Dozier,C.

PY - 2011

Y1 - 2011

N2 - Cdc25B phosphatases function as key players in G2/M cell cycle progression by activating the CDK1-cyclinB1 complexes. They also have an essential role in recovery from the G2/M checkpoint activated in response to DNA damage. Overexpression of Cdc25B results in bypass of the G2/M checkpoint and illegitimate entry into mitosis, and also causes replicative stress, leading to genomic instability. Thus, fine-tuning of Cdc25B expression level is critical for correct cell cycle progression and G2 checkpoint recovery. However, the transcriptional regulation of Cdc25B remains largely unknown. Earlier studies have shown that the tumor suppressor p53 overexpression transcriptionally represses Cdc25B; however, the molecular mechanism of this repression has not yet been elucidated, although it was suggested to occur through the induction of p21. Here we show that Cdc25B is downregulated by the basal level of p53 in multiple cell types. This downregulation also occurs in p21/ cell lines, indicating that p21 is not required for p53-mediated regulation of Cdc25B. Deletion and mutation analyses of the Cdc25B promoter revealed that downregulation by p53 is dependent on the presence of functional Sp1/Sp3 and NF-Y binding sites. Furthermore, chromatin immunoprecipitation analyses show that p53 binds to the Cdc25B promoter and mediates transcriptional attenuation through the Sp1 and NF-Y transcription factors. Our results suggest that the inability to downregulate Cdc25B after loss of p53 might contribute to tumorigenesis. © 2011 Macmillan Publishers Limited All rights reserved.

AB - Cdc25B phosphatases function as key players in G2/M cell cycle progression by activating the CDK1-cyclinB1 complexes. They also have an essential role in recovery from the G2/M checkpoint activated in response to DNA damage. Overexpression of Cdc25B results in bypass of the G2/M checkpoint and illegitimate entry into mitosis, and also causes replicative stress, leading to genomic instability. Thus, fine-tuning of Cdc25B expression level is critical for correct cell cycle progression and G2 checkpoint recovery. However, the transcriptional regulation of Cdc25B remains largely unknown. Earlier studies have shown that the tumor suppressor p53 overexpression transcriptionally represses Cdc25B; however, the molecular mechanism of this repression has not yet been elucidated, although it was suggested to occur through the induction of p21. Here we show that Cdc25B is downregulated by the basal level of p53 in multiple cell types. This downregulation also occurs in p21/ cell lines, indicating that p21 is not required for p53-mediated regulation of Cdc25B. Deletion and mutation analyses of the Cdc25B promoter revealed that downregulation by p53 is dependent on the presence of functional Sp1/Sp3 and NF-Y binding sites. Furthermore, chromatin immunoprecipitation analyses show that p53 binds to the Cdc25B promoter and mediates transcriptional attenuation through the Sp1 and NF-Y transcription factors. Our results suggest that the inability to downregulate Cdc25B after loss of p53 might contribute to tumorigenesis. © 2011 Macmillan Publishers Limited All rights reserved.

KW - Cdc25B

KW - p53

KW - Sp1

KW - NF-Y

KW - CELL-CYCLE REGULATION

KW - WILD-TYPE P53

KW - BREAST-CANCER

KW - DNA-DAMAGE

KW - EXPRESSION

KW - ACTIVATION

KW - PHOSPHATASE

KW - APOPTOSIS

KW - GENES

KW - TRIGGERS

UR - http://www.scopus.com/inward/record.url?scp=79955847712&partnerID=8YFLogxK

U2 - 10.1038/onc.2010.588

DO - 10.1038/onc.2010.588

M1 - Article

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 19

VL - 30

SP - 2282

EP - 2288

ER -

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