C/EBPβ Participates in Regulating Transcription of the p53 Gene in Response to Mitogen Stimulation

Boggs, Kristy; Reisman, David

doi:10.1074/jbc.m611675200

Cited by 31 publications

(38 citation statements)

References 45 publications

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“…To further address the role of C/EBP β in p53 regulation, we conducted ChIP experiments on C/EBP β +/+ primary keratinocytes to determine whether C/EBP β was bound to the p53 promoter at a site reported to be a bona fide C/EBP binding site. 29 We were unable to demonstrate any binding of C/EBP β to this area of the p53 promoter. In addition, we did not observe any differential regulation by C/EBP β of a mouse p53 promoter reporter, which contained the 1.2 kb proximal region of the p53 promoter with or without the above-mentioned C/EBP site (data not shown).…”

Section: Resultsmentioning

confidence: 65%

C/EBPβ represses p53 to promote cell survival downstream of DNA damage independent of oncogenic Ras and p19Arf

Ewing

Zhu

et al. 2008

Cell Death Differ

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CCAAT/enhancer-binding protein-β (C/EBPβ) is a mediator of cell survival and tumorigenesis. When C/EBPβ−/− mice are treated with carcinogens that produce oncogenic Ras mutations in keratinocytes, they respond with abnormally elevated keratinocyte apoptosis and a block in skin tumorigenesis. Although this aberrant carcinogen-induced apoptosis results from abnormal upregulation of p53, it is not known whether upregulated p53 results from oncogenic Ras and its ability to induce p19Arf and/or activate DNA-damage response pathways or from direct carcinogen-induced DNA damage. We report that p19Arf is dramatically elevated in C/EBPβ−/− epidermis and that C/EBPβ represses a p19Arf promoter reporter. To determine whether p19Arf is responsible for the proapoptotic phenotype in C/EBPβ−/− mice, C/EBPβ−/−;p19Arf−/− mice were generated. C/EBPβ−/−;p19Arf−/− mice responded to carcinogen treatment with increased p53 and apoptosis, indicating p19Arf is not essential. To ascertain whether oncogenic Ras activation induces aberrant p53 and apoptosis in C/EBPβ−/− epidermis, we generated K14-ER:Ras; C/EBPβ−/− mice. Oncogenic Ras activation induced by 4-hydroxytamoxifen did not produce increased p53 or apoptosis. Finally, when C/EBPβ−/− mice were treated with differing types of DNA-damaging agents, including alkylating chemotherapeutic agents, they displayed aberrant levels of p53 and apoptosis. These results indicate that C/EBPβ represses p53 to promote cell survival downstream of DNA damage and suggest that inhibition of C/EBPβ may be a target for cancer cotherapy to increase the efficacy of alkylating chemotherapeutic agents.

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Section: Resultsmentioning

confidence: 65%

C/EBPβ represses p53 to promote cell survival downstream of DNA damage independent of oncogenic Ras and p19Arf

Ewing

Zhu

et al. 2008

Cell Death Differ

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“…reports showed that C/EBP␤ binds to and regulates the p53 promoter (17,18). Given the elevation of C/EBP␤-HDAC1 complexes during development of liver cancer, we hypothesized that these complexes might be involved in the repression of p53 and subsequent development of cancer.…”

Section: The P53-p21 and P53-e2f7 Pathways Of Inhibition Of Liver Promentioning

confidence: 99%

Transcriptional and Translational Regulation of C/EBPβ-HDAC1 Protein Complexes Controls Different Levels of p53, SIRT1, and PGC1α Proteins at the Early and Late Stages of Liver Cancer

Jin

Iakova

Jiang

et al. 2013

Journal of Biological Chemistry

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Background: Development of liver cancer involves alterations of multiple pathways of gene expression. Results: Translational activation of C/EBP␤-HDAC1 complexes represses p53, SIRT1, and PGC1␣, leading to liver cancer. Conclusion: Modulation of levels of C/EBP␤-HDAC1 complexes at different stages of cancer is involved in liver cancer. Significance: Understanding the mechanisms of liver cancer is a critical step for the development of therapeutic approaches for cancer.

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“…promoter and regulates its expression (Boggs and Reisman, 2006;Boggs and Reisman, 2007). In addition, STS increases the expression of C/EBPβ (Hecker et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Mood stabilizers commonly restore staurosporine-induced increase of p53 expression and following decrease of Bcl-2 expression in SH-SY5Y cells

Song

Boku

Nakagawa

et al. 2012

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Adult neurogenesis in dentate gyrus (DG) is involved in the action mechanism of mood stabilizers. However, it is poorly understood how mood stabilizers affect adult neurogenesis in DG. Neurogenesis consists of proliferation, survival (anti-apoptosis) and differentiation of neural precursor cells in adult DG. Using in vitro culture of adult rat DG-derived neural precursor cells (ADP), we have already shown that four mood stabilizers, such as lithium (Li), valproate (VPA), carbamazepine (CBZ) and lamotrigine (LTG), commonly decrease staurosporine (STS)-induced apoptosis of ADP. These suggest that the common anti-apoptotic effect of mood stabilizers could be involved in mood-stabilizing effects.Past studies have shown that Li and VPA increase the expression of Bcl-2, an anti-apoptotic gene. In addition, it has been shown that Li decreases the expression of p53, which plays a prominent role in apoptosis and regulates the expression of Bcl-2. Therefore, p53 and Bcl-2 can be considered to mediate the common anti-apoptotic effects of Li, VPA, CBZ and LTG.To elucidate the molecular mechanism underlying the common anti-apoptotic effects of mood stabilizers, we investigated the effects of Li, VPA, CBZ and LTG on STS-induced expression changes of p53, Bcl-2 and other p53-related molecules using SH-SY5Y cells as a model of neural precursor-like cells. STS increased the expression of p53 and decreased that of Bcl-2. These effects of STS on p53 and Bcl-2 are restored by all of Li, VPA, CBZ and LTG. In addition, p53 overexpression decreased the expression of Bcl-2. Taken together, these results suggest that p53 and Bcl-2 may be involved in a part of mood-stabilizing effects.

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C/EBPβ Participates in Regulating Transcription of the p53 Gene in Response to Mitogen Stimulation

Cited by 31 publications

References 45 publications

C/EBPβ represses p53 to promote cell survival downstream of DNA damage independent of oncogenic Ras and p19Arf

C/EBPβ represses p53 to promote cell survival downstream of DNA damage independent of oncogenic Ras and p19Arf

Transcriptional and Translational Regulation of C/EBPβ-HDAC1 Protein Complexes Controls Different Levels of p53, SIRT1, and PGC1α Proteins at the Early and Late Stages of Liver Cancer

Mood stabilizers commonly restore staurosporine-induced increase of p53 expression and following decrease of Bcl-2 expression in SH-SY5Y cells

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