Редактирование: EP300 (раздел)

==Publications==

{{medline-entry
|title=[[TRIM27]] Functions as a Novel Oncogene in Non-Triple-Negative Breast Cancer by Blocking Cellular Senescence through p21 Ubiquitination.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33251042
|abstract=In the current study, we aimed to explore the correlation between [[TRIM27]] and breast cancer prognosis, as well as the functions of [[TRIM27]] in breast cancer and their underlying mechanisms. Bioinformatics analyses were used to examine the correlation between [[TRIM27]] and breast cancer prognosis. Moreover, [[TRIM27]] knockdown and overexpression in breast cancer cells were performed to investigate its functions in breast cancer. Tamoxifen (TAM) was applied to evaluate the influence of [[TRIM27]] on chemoresistance of breast cancer cells, while co-immunoprecipitation (coIP) was performed to identify the E3 ubiquitin ligase capability of [[TRIM27]]. High expression of [[TRIM27]] was found in non-triple-negative breast cancer (non-TNBC) tumor tissues and was positively correlated with the mortality of non-TNBC patients. Moreover, [[TRIM27]] could suppress non-TNBC cell apoptosis and senescence, promote cell viability and tumor growth, counteract the anti-cancer effects of TAM, and mediate ubiquitination of p21. In addition, [[EP300]] could enhance the expression of [[TRIM27]] and its transcription promoter H3K27ac. [[TRIM27]], through ubiquitination of p21, might serve as a prognostic biomarker for non-TNBC prognosis. [[TRIM27]] functions as a novel oncogene in non-TNBC cellular processes, especially suppressing cell senescence and interfering with non-TNBC chemoresistance.

|keywords=* EP300
* TRIM27
* breast cancer
* cell apoptosis
* cell senescence
* chemoresistance
* p21
* prognosis
* transcription
* ubiquitination
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666371
}}
{{medline-entry
|title=Identification of key genes and transcription factors in aging mesenchymal stem cells by DNA microarray data.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30641220
|abstract=Mesenchymal stem cells ([[MSC]]s) are multipotent cells that can be widely used in stem cell therapy. However, few studies have revealed the potential mechanisms of the changes in aging [[MSC]]. In this study, microarray data GSE35955 was downloaded from the Gene Expression Omnibus database. Then limma package in R was used to filtrate differentially expressed genes (DEGs), Transcription factors ([[TF]]s) were predicted by DCGL package. After predicting [[TF]]s, protein-protein interaction (PPI) network and [[TF]]-mediated transcriptional regulation network were constructed. The functional and pathway enrichment analysis of screened DEGs, hub genes and [[TF]]s were conducted by the DAVID. Totally 156 up-regulated DEGs and 343 down-regulated DEGs were obtained. 6 hub genes ([[CTNNB1]], [[PPP2R1A]], [[FYN]], [[MAPK1]], [[PIK3C2A]] and [[EP300]]) were obtained from PPI network. 11 [[TF]]s (CREB1, [[[[CUX1]]]], [[EGR1]], [[EP300]], [[FOXC1]], [[HSF2]], [[MEF2A]], [[PLAU]], [[SP1]], [[STAT1]] and USF1) for DEGs were predicted and 2 highly scored co-expression relationships ([[EP300]]-[[PPP2R1A]] and [[STAT1]]-[[FOXC1]]) were acquired from the [[TF]]-mediated transcriptional regulation network. The discovery of the hub genes, [[TF]]s and pathways might contribute to the understanding of genetic and molecular functions of aging-related changes in [[MSC]]. Further validation studies on genes and [[TF]]s such as [[CTNNB1]], [[FYN]], [[PPP2R1A]], [[MAPK1]], [[EP300]] and related biological processes and pathways, including adherens junction, DNA damage caused from oxidative stress, attribution of telomere, [[MSC]] differentiation and epigenetic regulation, are urgent for clinical prevention and treatment.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Gene Expression Profiling
* Gene Expression Regulation
* Humans
* Mesenchymal Stem Cells
* Middle Aged
* Mitogen-Activated Protein Kinase 1
* Oligonucleotide Array Sequence Analysis
* Protein Interaction Maps
* Protein Phosphatase 2
* Proto-Oncogene Proteins c-fyn
* Transcription Factors
* beta Catenin
|keywords=* Differentially expressed genes
* Enrichment analysis
* Gene Expression Omnibus
* Hub genes
* Microarray analysis
* Protein-protein interaction network
* Transcriptional regulatory network
|full-text-url=https://sci-hub.do/10.1016/j.gene.2018.12.063
}}
{{medline-entry
|title=Aspirin-another caloric-restriction mimetic.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29929449
|abstract=The capacity of cells and organisms to sustain, and to eventually adapt to, environmental and genetic insults declines with age. Because macroautophagy/autophagy is regarded as one of the major determinants of cellular fitness in vitro and in vivo, maneuvers that aim at promoting autophagy may slow down aging and promote health span. Caloric restriction (CR), a reduction in caloric intake without malnutrition, efficiently counteracts aging-associated features, yet is difficult to be applied to humans. Caloric-restriction mimetics (CRMs) are pharmacological agents that recapitulate the main biochemical properties of CR, namely a global reduction of protein acetylation and the induction of autophagy. We found that the ancient drug aspirin and its active metabolite salicylate stimulate autophagic flux by virtue of their inhibitory action on acetyltransferase [[EP300]]. The inhibition of [[EP300]] results from a direct competition between salicylate and acetyl coenzyme A for binding to the catalytic domain of the enzyme. This mode of action appears to be conserved across evolution as it accounts for the induction of autophagy by aspirin in various mouse models and in the nematode [i]Caenorhabditis elegans[/i]. In sum, aspirin acts as a CRM.
|mesh-terms=* Acetyl Coenzyme A
* Animals
* Aspirin
* Autophagy
* Caenorhabditis elegans
* Caloric Restriction
* Humans
* Mice
|keywords=* AMPK
* Acetylation
* aging
* autophagy
* fasting
* inflammation
* longevity
* mitophagy
* salicylate
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6103658
}}
{{medline-entry
|title=Aspirin Recapitulates Features of Caloric Restriction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29490275
|abstract=The age-associated deterioration in cellular and organismal functions associates with dysregulation of nutrient-sensing pathways and disabled autophagy. The reactivation of autophagic flux may prevent or ameliorate age-related metabolic dysfunctions. Non-toxic compounds endowed with the capacity to reduce the overall levels of protein acetylation and to induce autophagy have been categorized as caloric restriction mimetics (CRMs). Here, we show that aspirin or its active metabolite salicylate induce autophagy by virtue of their capacity to inhibit the acetyltransferase activity of [[EP300]]. While salicylate readily stimulates autophagic flux in control cells, it fails to further increase autophagy levels in [[EP300]]-deficient cells, as well as in cells in which endogenous [[EP300]] has been replaced by salicylate-resistant [[EP300]] mutants. Accordingly, the pro-autophagic activity of aspirin and salicylate on the nematode Caenorhabditis elegans is lost when the expression of the [[EP300]] ortholog cpb-1 is reduced. Altogether, these findings identify aspirin as an evolutionary conserved CRM.
|mesh-terms=* Acetyl Coenzyme A
* Animals
* Aspirin
* Autophagy
* Caloric Restriction
* Cell Line, Tumor
* E1A-Associated p300 Protein
* Humans
* Metabolome
* Metabolomics
* Mice, Inbred C57BL
|keywords=* EP300
* acetylation
* aging
* autophagy
* longevity
* metabolome
* salicylate
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5848858
}}