Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The CCAAT/enhancer binding protein alpha (C/EBPalpha or CEBPA) is the founding member of a family of related leucine zipper transcription factors that play important roles in myeloid differentiation. Targeted inactivation of C/EBPalpha in mice demonstrates its importance in the proper development and function of liver, adipose tissue, lung and haematopoietic tissues. C/EBPalpha is highly expressed in these differentiated tissues where it controls differentiation-dependent gene expression and inhibits cell proliferation. Learning more about the precise molecular functions of the C/EBPalpha protein and how these are affected by leukaemogenic mutations should lead to an improved understanding of the cellular functions that are disrupted in patients with AML. Decreased expression of C/EBPalpha but not C/EBPalpha mutation has been shown in patients with granulocytic leukaemias that are associated with translocations t(8;21), inv (16) or t(15;17). Derived fusion proteins repress C/EBPalpha expression. Differentiation therapy of some AML types is based on restoring C/EBPalpha function. However, apparently normal C/EBPalpha is overexpressed in BCP-ALL harbouring the translocation t(14; 19)(q32; q13). C/EBPalpha may exhibit oncogenic as well as tumour suppressor properties in human leukaemogenesis. C/EBPalpha mutations were not found in non-haematopoietic cancers. DNA hypermethylation of the upstream C/EBPalpha promoter region is responsible for very low C/EBPalpha expression in human lung and endometrial cancer. C/EBPalpha expression may be a biomarker for early detection of these cancers and DNA-modifying drugs such as demethylating agents and/or histone deacetylase inhibitors could be used in the treatment of these malignancies.
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PMID:Growth-inhibiting activity of transcription factor C/EBPalpha, its role in haematopoiesis and its tumour suppressor or oncogenic properties in leukaemias. 1758

We evaluated the effect of bisphenol A and its metabolites on the 3T3-L1 cells, in terms of glucose and lipid metabolism. We also aimed to obtain the information on the genome-wide expression changes in the 3T3-L1 cells treated with Bisphenol A by using RNA-seq, which involves whole-transcriptome sequencing. Differentially Expressed Genes (DEGs) collected from RNA-seq can be used to produce a complete picture of related metabolism pathways. The KEGG pathway was extracted based on the DEGs. Bisphenol A significantly increased the mRNA level of Sterol regulatory element binding transcription factor 1 (Srebf1) and CCAAT/enhancer binding protein alpha (Cebpa). Lipoprotein lipase (Lpl) was also significantly influenced by bisphenol A and its metabolites. Acetyl-Coenzyme A carboxylase beta (Acacb) and Fatty acid synthase (Fasn) mRNA levels were elevated by bisphenol A and its metabolites. The insulin signaling pathway, neurotrophin signaling pathway, and endometrial cancer-related pathway were focused by the functional enrichment analyses, and the pathways were well coincided with recent previous reports. DEGs collected from RNA-seq were confirmed as a reliable evidence in the exposure to the chemicals such as bisphenol A. Collecting pieces of the puzzles obtained from the RNA-seq will help us to produce a complete picture of the metabolic pathway for such chemicals.
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PMID:Identification of metabolic pathways related to the bisphenol A-induced adipogenesis in differentiated murine adipocytes by using RNA-sequencing. 3066 18