C/EBPβ: lost beyond translation

Peeper, Daniel S.

doi:10.1038/emboj.2011.288

Cited by 7 publications

(6 citation statements)

References 12 publications

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“…The C/EBP b (also known as CEBPB) is a basic leucine zipper transcription factor that regulates a variety of biological processes, including metabolism, cell proliferation and differentiation, and immune response (11)(12)(13). Recent findings show that C/EBP binduced inflammatory responses mediate KA-triggered excitotoxic brain injury (10).…”

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confidence: 99%

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Lü

Zheng

et al. 2013

The Journal of Immunology

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The C/EBP β is a basic leucine zipper transcription factor that regulates a variety of biological processes, including metabolism, cell proliferation and differentiation, and immune response. Recent findings show that C/EBP β–induced inflammatory responses mediate kainic acid–triggered excitotoxic brain injury. In this article, we show that protein kinase C ζ enhances K-ras expression and subsequently activates the Raf/MEK/ERK1/2 pathway in the hippocampus of domoic acid (DA)–treated mice, which promotes C/EBP β expression and induces inflammatory responses. Elevated production of TNF-α impairs mitochondrial function and increases the levels of reactive oxygen species by IκB kinase β/NF-κB signaling. The aforementioned inflammation and oxidative stress lead to memory deficits in DA-treated mice. However, troxerutin inhibits cyclin-dependent kinase 1 expression, enhances type 1 protein phosphatase α dephosphorylation, and abolishes MEK/ERK1/2/C/EBP β activation, which subsequently reverses the memory impairment observed in the DA-treated mice. Thus, troxerutin is recommended as a potential candidate for the prevention and therapeutic treatment of cognitive deficits resulting from excitotoxic brain damage and other brain disorders.

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confidence: 99%

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Lü

Zheng

et al. 2013

The Journal of Immunology

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“…The transcription factor CEBPB is a basic leucine zipper DNAbinding domain protein that regulates the proliferation and differentiation of various cell types. 38 Previous studies [39][40][41] have primarily focused on the critical role of CEBPB in cellular senescence. However, several studies [42][43][44] have also observed an association between CEBPB and pro-apoptotic processes.…”

Section: Discussionmentioning

confidence: 99%

Assessing the double‐edged of extracellular signal‐regulated kinase/CCAAT‐enhancer‐binding protein beta signaling pathway in arsenic‐induced skin damage and its potential foodborne interventions

Yang

et al. 2023

Environmental Toxicology

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Arsenic exposure is a major environmental public health challenge worldwide. As typical manifestations for arsenic exposure, the pathogenesis of arsenic‐induced skin lesions has not been fully elucidated, as well as the lack of effective control measures. In this study, we first determined the short‐term and high‐dose arsenic exposure can increase the apoptosis rates, while long‐term low‐dose arsenic exposure decrease the apoptosis rates. Then, the HaCaT cells with knockdown and overexpression of CCAAT‐enhancer‐binding protein β (CEBPB) and extracellular signal‐regulated kinase (ERK) were constructed. The results demonstrate that knockdown of CEBPB and ERK can reduce NaAsO2‐induced cell apoptosis by inhibiting ERK/CEBPB signaling pathway and vice versa. Further cells were treated with Kaji‐Ichigoside F1 (KF1). The results clearly show that KF1 can decrease the arsenic‐induced cell apoptosis rates and the expression of ERK/CEBPB signaling pathway‐related genes. These results provide evidence that ERK/CEBPB signaling pathway acts as a double‐edged sword in arsenic‐induced skin damage. Another interesting finding was that KF1 can alleviate arsenic‐induced skin cell apoptosis by inhibiting the ERK/CEBPB signaling pathway. This study will contribute to a deeper understanding of the mechanisms of arsenic‐induced skin cell apoptosis, and our findings will help to identify a potential food‐borne intervention in arsenic detoxification.

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“…In nasopharyngeal carcinoma and HNSCC, CEBPB is involved in PGC1α-mediated radiation resistance [ 17 , 34 ]. The abnormal translation of CEBPB [ 35 ] has been widely reported in macrophage migration [ 36 ], metabolic diseases [ 37 ] and leukemia [ 38 ]. EIF6 was previously described as a CEBPB translational regulator, mainly in adipogenic regulation [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Eukaryotic translation initiation factor 3 subunit B promotes head and neck cancer via CEBPB translation

Shi

Zhang

et al. 2022

Cancer Cell Int

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Background Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer type worldwide. Deregulation of mRNA translation is a frequent feature of cancer. Eukaryotic translation initiation factor 3 subunit B (EIF3B) has been reported as an oncogene; however, its role in HNSCC has yet to be fully elucidated. Methods In this study, the clinical significance of EIF3B expression was analyzed based on TCGA datasets. Then, EIF3B expression was knocked down and its role in HNSCC was revealed. To explore the molecular mechanisms of EIF3B, we applied RNA sequencing and proteomics and acquired deregulated pathways. RNA immunoprecipitation (RIP) sequencing was conducted to reveal the target mRNAs of EIF3B, and TCGA datasets were used to validate potential targets of EIF3B. Results Elevated expression of EIF3B was observed in the HNSCC cancer samples. The expression of EIF3B was significantly correlated with the patient’s sex, age, HPV infection status, T stage, N stage, perineural invasion status and survival status. EIF3B serves as a marker of an unfavorable HNSCC prognosis. EIF3B-silenced Fadu and Cal27 cells exhibited reduced cell numbers, and EIF3B knockdown induced apoptosis in both cell lines. The EIF3B-silenced cells demonstrated decreased invasion and migration capabilities, and the EIF3B knockdown group mice showed significantly decreased tumor volumes. The results show that EIF3B promotes CEBPB translation and activates the MAPK pathway and revealed that IL6R and CCNG2 are targets of EIF3B-regulated CEBPB translation. Conclusion In summary, the results indicated that EIF3B is a novel oncogene in HNSCC that promotes CEBPB translation and IL6R expression, and these findings provide a link between the molecular basis and pathogenesis of HNSCC. Graphical Abstract

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C/EBPβ: lost beyond translation

Cited by 7 publications

References 12 publications

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Assessing the double‐edged of extracellular signal‐regulated kinase/CCAAT‐enhancer‐binding protein beta signaling pathway in arsenic‐induced skin damage and its potential foodborne interventions

Eukaryotic translation initiation factor 3 subunit B promotes head and neck cancer via CEBPB translation

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