Differential induction of growth arrest inducible genes by selenium compounds

Kaeck, Mark; Lü, Junxuan; Strange, Robert; Ip, Clement; Ganther, Howard E.; Thompson, Henry J.

doi:10.1016/s0006-2952(97)00103-2

Cited by 89 publications

(67 citation statements)

References 13 publications

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“…26 A temperature-sensitive p53 plasmid was transfected into the MOD cells. This plasmid generates a p53 protein that is inactive at 378C, but by incubating these cells at the permissive temperature of 308C, the transfected p53 behaves as wildtype and is activated.…”

Section: Results P53 Induces Apoptosis At the Permissive Temperaturementioning

confidence: 99%

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DNA repair is activated in early stages of p53-induced apoptosis

et al. 2000

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Abstractp53 is a complex molecule involved in apoptosis, cell cycle arrest, and DNA repair. Since apoptosis may play an important role in deletion of neoplastic cells, an understanding of the mechanism of p53-induced apoptosis may be critical for possible future therapeutic interventions. Recent evidence suggests that p53-induced apoptosis may involve members of the nucleotide excision repair (NER) family, linking these two cellular events. Our work using a temperature-sensitive p53 construct further analyzes p53-induced apoptosis in cultured murine mammary epithelial cells and also suggests that DNA repair plays a role in that process. Although p21 is induced in our system, apoptosis occurs without a detectable preceding G1 cell cycle arrest and independent of cellular alterations brought on by the temperature shift. In addition, clonogenic assays suggest that early stages of p53-induced apoptosis may be reversible upon removal of the apoptosis stimulus. As a possible explanation for this reversibility, our results show that general DNA repair activity increases early in p53-induced apoptosis. We also show that caspase-3 is activated at a timepoint when colony formation begins to drop, suggesting a possible mechanism for the point of no return in p53-induced apoptosis. Cell Death and Differentiation (2000) 7, 393 ± 401.

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Section: Results P53 Induces Apoptosis At the Permissive Temperaturementioning

confidence: 99%

“…26 We stably transfected these cells with either a temperature-sensitive p53 plasmid (p53ts) or a constitutively mutant p53 (p53mut). The p53ts plasmid results in a valine substituted for alanine at amino acid #135 of the mouse protein, while the p53mut construct contains a cysteine to phenylalanine substitution at amino acid #132.…”

Section: Methodsmentioning

confidence: 99%

DNA repair is activated in early stages of p53-induced apoptosis

et al. 2000

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“…The fact that modulation of NKG2D ligands is restricted to CH 3 SeH-generating compounds is especially interesting for treatment approaches because H 2 Se metabolites are associated with genotoxic effects in cells (86,87). Therefore, this so far unrecognized immune regulatory effect caused by CH 3 SeH-generating compounds should be added to the list of chemopreventive potential mediated by selenium compounds, and in particular considered for implementation in the treatment of NKG2D ligand-expressing tumors or adjuvant therapy in general.…”

Section: Discussionmentioning

confidence: 99%

The Selenium Metabolite Methylselenol Regulates the Expression of Ligands That Trigger Immune Activation through the Lymphocyte Receptor NKG2D

Hagemann-Jensen

Uhlenbrock

Kehlet

et al. 2014

Journal of Biological Chemistry

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Background: Immune activation through a balanced cell surface expression of human NKG2D ligands is crucial for the elimination of diseased cells. Results: Methylselenol induces the expression of the NKG2D ligands MICA/B but specifically inhibits ULBP2 protein expression. Conclusion: Methylselenol regulates NKG2D ligand expression on transcriptional and posttranscriptional levels. Significance: Methylselenol is the first identified metabolite that diversely regulates NKG2D ligands, and, therefore, its implementation could improve NKG2D-based immune therapy.

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“…One such gene, Gadd153 (also known as chop), encodes a member of the CCAAT\enhancer-binding protein (C\EBP) family of transcription factors. Originally isolated based on its induction by UV-C irradiation [1], Gadd153 has subsequently been shown to be highly induced in a variety of stress paradigms that result in growth arrest or DNA damage, including genotoxic agents [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16], calcium ionophore [17], nutrient depletion [15,[18][19][20], oxidative stress [21][22][23], reductive stress [24,25], endoplasmic reticulum stress [26][27][28] and the acute-phase response [29,30]. GADD153 (where GADD stands for growth arrest and DNA damage-inducible protein) has been implicated in the commitment to, or implementation of, growth arrest or cell death ; microinjection of GADD153 induces 3T3 cells to arrest at the G " \S boundary [31], while ectopic expression of GADD153 causes M1 myeloblastic leukaemia cells to undergo apoptosis [32].…”

Section: Introductionmentioning

confidence: 99%

Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)–ATF composite site to regulate Gadd153 expression during the stress response

Fawcett

Martindale

Guyton

et al. 1999

Biochemical Journal

378

229

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Gadd153, also known as chop, encodes a member of the CCAAT/enhancer-binding protein (C/EBP) transcription factor family and is transcriptionally activated by cellular stress signals. We recently demonstrated that arsenite treatment of rat pheochromocytoma PC12 cells results in the biphasic induction of Gadd153 mRNA expression, controlled in part through binding of C/EBPβ and two uncharacterized protein complexes to the C/EBP–ATF (activating transcription factor) composite site in the Gadd153 promoter. In this report, we identified components of these additional complexes as two ATF/CREB (cAMP-responsive-element-binding protein) transcription factors having differential binding activities dependent upon the time of arsenite exposure. During arsenite treatment of PC12 cells, we observed enhanced binding of ATF4 to the C/EBP–ATF site at 2 h as Gadd153 mRNA levels increased, and enhanced binding of ATF3 complexes at 6 h as Gadd153 expression declined. We further demonstrated that ATF4 activates, while ATF3 represses, Gadd153 promoter activity through the C/EBP–ATF site. ATF3 also repressed ATF4-mediated transactivation and arsenite-induced activation of the Gadd153 promoter. Our results suggest that numerous members of the ATF/CREB family are involved in the cellular stress response, and that regulation of stress-induced biphasic Gadd153 expression in PC12 cells involves the ordered, sequential binding of multiple transcription factor complexes to the C/EBP–ATF composite site.

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Differential induction of growth arrest inducible genes by selenium compounds

Cited by 89 publications

References 13 publications

DNA repair is activated in early stages of p53-induced apoptosis

DNA repair is activated in early stages of p53-induced apoptosis

The Selenium Metabolite Methylselenol Regulates the Expression of Ligands That Trigger Immune Activation through the Lymphocyte Receptor NKG2D

Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)–ATF composite site to regulate Gadd153 expression during the stress response

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