Repression of mRNA for the PLK cell cycle gene after DNA damage requires BRCA1

Ree, Anne Hansen; Bratland, Åse; Nome, Ragnhild V.; Stokke, Trond; Fodstad, Øystein

doi:10.1038/sj.onc.1207000

Cited by 33 publications

(37 citation statements)

References 27 publications

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“…PLK1 regulates the activity of CDC2-cyclin B by phosphorylating CDC25C in a TP53 independent manner. 21,22 Moreover, decreased expression of CCNF in both lines may have contributed to the arrest as well since cyclin F probably is a positive regulator of the nuclear localization of cyclin B1. 23 TP53, on the other hand, played probably no role in the G 2 arrest, since repression of TP53 function in our ongoing studies had no influence on this phenotype, as mentioned above.…”

Section: Discussionmentioning

confidence: 99%

Response of malignant B lymphocytes to ionizing radiation: Gene expression and genotype

Lyng

Landsverk

Kristiansen

et al. 2005

Intl Journal of Cancer

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The human malignant B-lymphocyte cell lines Reh and U698 show arrest in G 2 phase after ionizing radiation (IR), but only Reh cells arrest in G 1 phase and die by apoptosis. We have used cDNA microarrays to measure changes in gene expression at 2, 4 and 6 hr after irradiation of Reh and U698 cells with 0.5 and 4 Gy in order to begin exploring the molecular mechanisms underlying the phenotypic changes. We also investigated whether gene expression changes could be caused by possible aberrations of genes, as measured by comparative genomic hybridization. Reh cells showed upregulation of CDKN1A that likely mediated the G 1 arrest. In contrast, U698 cells have impaired function of TP53 protein and no activation of CDKN1A, suppressing the arrest in G 1 . The G 2 arrest in both cell lines was likely due to repression of PLK1 and/or CCNF. IR-induced apoptosis in Reh cells was probably mediated by TP53 and CDKN1A, whereas a high expression level of MCL1, caused by gene amplification, and activation of the NFKB pathway may have suppressed the apoptotic response in U698 cells. Genes suggested to be involved in apoptosis were activated long before this phenotype was detectable and showed the same temporal expression profiles as genes involved in cell cycle arrest. Our results suggest that differences in functionality and/or copy number of several genes involved in IR-regulated pathways contributed to the phenotypic differences between Reh and U698 cells after IR, and that multiple molecular factors control the radiation response of malignant B lymphocytes. ' 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Response of malignant B lymphocytes to ionizing radiation: Gene expression and genotype

Lyng

Landsverk

Kristiansen

et al. 2005

Intl Journal of Cancer

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“…Recently, Ree et al (51) found that ionizing radiation leads to the suppression of Plk1 mRNA expression. It is of interest to examine whether genotoxic stresses other than cisplatin and ionizing radiation could also repress the expression of Plk1.…”

Section: Discussionmentioning

confidence: 99%

Polo-like Kinase 1 (Plk1) Inhibits p53 Function by Physical Interaction and Phosphorylation

Ando

Ozaki

Yamamoto

et al. 2004

Journal of Biological Chemistry

247

237

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Polo-like kinase 1 (Plk1) has an important role in the regulation of M phase of the cell cycle. In addition to its cell cycle-regulatory function, Plk1 has a potential role in tumorigenesis. Here we found for the first time that Plk1 physically binds to the tumor suppressor p53 in mammalian cultured cells, and inhibits its transactivation activity as well as its pro-apoptotic function. During the cisplatin-induced apoptosis in human neuroblastoma SH-SY5Y cells, the expression level of Plk1 was significantly decreased both at mRNA and protein levels, whereas cisplatin treatment caused a remarkable stabilization of p53. Systematic immunoprecipitation analyses using a series of deletion mutants of p53 revealed that a sequence-specific DNA-binding region of p53 is required and sufficient for the physical interaction with Plk1. The ectopically overexpressed Plk1 was co-localized with the endogenous p53 in mammalian cell nucleus, as shown by confocal laser microscopy. Expression of exogenous Plk1 and p53 in p53-deficient lung carcinoma H1299 cells greatly decreased the p53-mediated transcription from the p53-responsive p21 WAF1 , MDM2, and BAX promoters, whereas the kinase-deficient mutant form of Plk1 failed to reduce the transcriptional activity of p53. Consistent with the luciferase reporter analysis, Plk1 had an ability to block the p53-dependent induction of the endogenous p21 WAF1 . In addition, Plk1 inhibited the pro-apoptotic function of p53 in H1299 cells. Intriguingly, Plk1-mediated repression of p53 was attenuated with ATM. Thus, our present findings strongly suggest that p53 is a critical target of Plk1, and its function is abrogated through the physical interaction with Plk1.

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“…For example, Plk1 expression increases when the mitogen phytohemagglutinin is added to human peripheral blood lymphocytes (Holtrich et al, 1994;Yuan et al, 1997), but decreases during nerve growth factor-induced rat PC12 cell differentiation (Hamanaka et al, 1994), during phorbol myristate acetate (PMA)-induced human U937 and HL-60 monocytic cell differentiation (Yuan et al, 1997), and when human glioma cell growth is inhibited using antisense oligonucleotides targeting phospholipase C-gamma mRNA (Dietzmann et al, 2002). Also, DNA-damaging agents that promote cell cycle arrest have been reported to decrease Plk1 gene expression levels in mammalian cells (Ree et al, 2003;Ando et al, 2004). In breast cancer cells, ionizing radiation-induced Plk1 mRNA downregulation is dependent on CHEK1 signaling and BRCA1 function (Ree et al, 2003).…”

Section: Cells In Culturementioning

confidence: 99%

“…Also, DNA-damaging agents that promote cell cycle arrest have been reported to decrease Plk1 gene expression levels in mammalian cells (Ree et al, 2003;Ando et al, 2004). In breast cancer cells, ionizing radiation-induced Plk1 mRNA downregulation is dependent on CHEK1 signaling and BRCA1 function (Ree et al, 2003).…”

Section: Cells In Culturementioning

confidence: 99%

Differential regulation of polo-like kinase 1, 2, 3, and 4 gene expression in mammalian cells and tissues

Winkles

Alberts²

2005

Oncogene

139

123

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Repression of mRNA for the PLK cell cycle gene after DNA damage requires BRCA1

Cited by 33 publications

References 27 publications

Response of malignant B lymphocytes to ionizing radiation: Gene expression and genotype

Response of malignant B lymphocytes to ionizing radiation: Gene expression and genotype

Polo-like Kinase 1 (Plk1) Inhibits p53 Function by Physical Interaction and Phosphorylation

Differential regulation of polo-like kinase 1, 2, 3, and 4 gene expression in mammalian cells and tissues

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