TIP30 Directly Binds p53 Tumor Suppressor Protein In Vitro

Lee, Si Hyung; Ju, Sung-Kyu; Lee, Tae Young; Huh, Sung-Ho; Han, Kyou‐Hoon

doi:10.1007/s10059-012-0232-x

Cited by 10 publications

(10 citation statements)

References 29 publications

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“…For instance, TIP30 has a significant effect on DNA repair after ultraviolet light and oxidant exposure, and can regulate the metabolic adaptation of tumor cells to glucose limitations [29,30]. Moreover, TIP30 regulates p53 at the protein level by directly binding to it, and it might regulate the BAX gene partly through directly binding to p53 protein, which sensitizes cells to apoptosis by involving a p53 apoptosis signal transduction pathway [31,32]. Researchers also showed that TIP30 could inhibit snail-mediated epithelial-mesenchymal transition (EMT) and tumor-initiating properties in hepatocellular carcinoma and suppress TGF-β1-induced EMT via AKT/β-catenin signaling in esophageal carcinoma[12,20].…”

Section: Discussionmentioning

confidence: 99%

Tat-Interacting Protein 30 (TIP30) Expression Serves as a New Biomarker for Tumor Prognosis: A Systematic Review and Meta-Analysis

Jin

Yuan

et al. 2016

PLoS ONE

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BackgroundTat-interacting protein 30 (TIP30) is a tumor suppressor protein that has been found to be expressed in a wide variety of tumor tissues. TIP30 is involved in the control of cell apoptosis, growth, metastasis, angiogenesis, DNA repair, and tumor cell metabolism. The methylation of the TIP30 promoter is also associated with tumor prognosis. To evaluate this topic further, we conducted a systematic meta-analysis to explore the clinicopathological and prognostic significance of TIP30 for tumor patients.MethodsWe searched PubMed and EMBASE for eligible studies. We manually searched for printed journals and relevant textbooks. Subgroup analyses were performed based on the region, manuscript quality, methods of vasculogenic mimicry identification, pathology, and number of patients.ResultsFourteen studies with 1705 patients were included in this meta-analysis. A significant association was observed between high expression of TIP30 in patients with cancer with a good overall survival (hazard ratio = 0.53, 95% confidence interval: 0.41–0.69), and good recurrence-free survival or disease free survival (hazard ratio = 0.49, 95% confidence interval: 0.37–0.66). Lack of expression of TIP30 had an association with lymph node metastasis (odds ratio = 3.90, 95% confidence interval: 2.21–6.89) and high tumor node metastasis clinical stage (odds ratio = 2.10, 95% confidence interval: 1.68–2.62). The methylation of the TIP30 promoter did not significantly influence the overall survival (hazard ratio = 0.99, 95% confidence interval: 0.88–1.13) or disease free survival (hazard ratio = 0.62, 95% confidence interval: 0.19–2.02).ConclusionsTIP30 expression is associated with a good prognosis in patients with tumors. Clinical studies with large samples are needed worldwide and standardized protocols should be adopted in the future to achieve a better understanding of the relationship between tumor prognosis and TIP30.

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Section: Discussionmentioning

confidence: 99%

Tat-Interacting Protein 30 (TIP30) Expression Serves as a New Biomarker for Tumor Prognosis: A Systematic Review and Meta-Analysis

Jin

Yuan

et al. 2016

PLoS ONE

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“…It has been shown that TIP30 stabilizes p53 mRNA and binds directly to the DNA-binding and C-terminal domain of p53. 43 Accordingly, the silencing of these genes is likely to influence lymphomagenesis directly.…”

Section: Integrative Analysis Of Gene Expression and Dna Methylationmentioning

confidence: 99%

Genome-wide profiling identifies a DNA methylation signature that associates with TET2 mutations in diffuse large B-cell lymphoma

et al. 2013

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The discovery that the Ten-Eleven Translocation (TET) hydroxylases cause DNA demethylation has fundamentally changed the notion of how DNA methylation is regulated. Clonal analysis of the hematopoetic stem cell compartment suggests that TET2 mutations can be early events in hematologic cancers and recent investigations have shown TET2 mutations in diffuse large B-cell lymphoma. However, the detection rates and the types of TET2 mutations vary, and the relation to global methylation patterns has not been investigated. Here, we show TET2 mutations in 12 of 100 diffuse large B-cell lymphomas with 7% carrying loss-of-function and 5% carrying missense mutations. Genome-wide methylation profiling using 450K Illumina arrays identified 315 differentially methylated genes between TET2 mutated and TET2 wild-type cases. TET2 mutations are primarily associated with hypermethylation within CpG islands (70%; P<0.0001), and at CpG-rich promoters (60%; P<0.0001) of genes involved in hematopoietic differentiation and cellular development. Hypermethylated loci in TET2 muta ted samples overlap with the bivalent (H3K27me3/H3K4me3) silencing mark in human embryonic stem cells (P=1.5x10 -30 ). Surprisingly, gene expression profiling showed that only 11% of the hypermethylated genes were down-regulated, among which there were several genes previously suggested to be tumor suppressors. A metaanalysis suggested that the 35 hypermethylated and down-regulated genes are associated with the activated B-celllike type of diffuse large B-cell lymphoma in other studies. In conclusion, our data suggest that TET2 mutations may cause aberrant methylation mainly of genes involved in hematopoietic development, which are silenced but poised for activation in human embryonic stem cells.Genome-wide profiling identifies a DNA methylation signature that associates with TET2 mutations in diffuse large B-cell lymphoma

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“…The interaction between p53 DBD and GFP was diminished in the absence of the HIS-tag. This result casts doubt on studies demonstrating a direct interaction between p53 and a HIStagged protein [43][44][45][46]. The interactions shown in these experiments could result from a true direct interaction or from artificial dimer formation between the HIS-tag and p53 zinc finger.…”

Section: Discussionmentioning

confidence: 75%

P53 and HIS-tag Binding

Barron¹,

Bishop²

2018

J Proteomics Bioinform

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P53 is a globular protein with distinct domains and a key tumor suppressor that functions through transcriptional transactivation, repression and protein-protein interactions. Numerous studies have implicated protein-protein interactions between p53 and a multitude of cellular proteins with a variety of known functions. Because of these interactions, and the many gene expression regulations, a multitude of potential mechanisms and their relationship to tumor suppression have been proposed. It is desirable to test these interactions in an in vitro setting to demonstrate that any identified interaction is direct. Due to the difficulties associated with purifying recombinant full-length p53, many studies have utilized the p53 DNA binding domain to test for direct protein interactions with p53. The DNA binding domain of p53 is structured, folds independently and dictates the stability of the full-length protein. Therefore, it is reasonable to perform in vitro experiments with this isolated domain. However, we demonstrate that if a HIStag is present on the interacting partner when testing for an interaction with p53, this can lead to detection of an artefactual protein-protein interaction raising the possibility of false positive results. Furthermore, the presence of the HIS-tag promotes aggregation and precipitation of the p53 DNA binding domain.

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TIP30 Directly Binds p53 Tumor Suppressor Protein In Vitro

Cited by 10 publications

References 29 publications

Tat-Interacting Protein 30 (TIP30) Expression Serves as a New Biomarker for Tumor Prognosis: A Systematic Review and Meta-Analysis

Tat-Interacting Protein 30 (TIP30) Expression Serves as a New Biomarker for Tumor Prognosis: A Systematic Review and Meta-Analysis

Genome-wide profiling identifies a DNA methylation signature that associates with TET2 mutations in diffuse large B-cell lymphoma

P53 and HIS-tag Binding

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