Transcriptomic analysis of 5637 bladder cancer cell line transfected with MAT1A plamid, 48 hours post transfection
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE133123 | GEO | 2019/06/22
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptomic analysis of 5637 bladder cancer cell line transfected with MAT1A plamid, 48 hours post transfection
| PRJNA550034 | ENA
Project description:In order to investigate epigenetic landscape and potential alterations in bladder, we established the chromatin profiling of 5637 cell line by ChIPseq for the following marks and transcription factor : H3K4me3, H3K9ac, H3K27me3, H3K9me3, H3K27ac, H3K4me1, CTCF and FOXA1.
2023-03-22 | GSE193811 | GEO
Project description:To identification of key drivers involved in the development of muscle invasive bladder cancer, which displays poor prognosis, we isolated one subpopulation of human 5637 bladder cancer cells with highly invasiveness and the other subpopulation of 5637 cells with low invasiveness by Transwell method. Through proteomic analysis, differentially expressed proteins were displayed.
2018-03-15 | PXD007709 | Pride
Project description:We knockdowned OMD and PRELP expression by specific siRNAs in 5637 bladder carcinoma cells and conducted expression profile analysis. We also overexpressed OMD and PRELP in T-REx 293 cells and conducted expression profile analysis.
2016-04-30 | GSE63955 | GEO
Project description:Methionine adenosyltransferase (MAT) enzymes generate SAMe (S-adenosylmethionine), the main biological methyl donor. There are two MAT encoding genes in mammals (Mat1a and Mat2a), which show different activities and cellular distribution. Mat1a encodes the enzyme mainly expressed in normal liver. Mat1a ablation in mice results in the spontaneous development of non-alcoholic steatohepatitis (NASH). We observed that SAMe depletion in Mat1a KO mice had three main effects on hepatic lipid metabolism: 1) impaired TG (triglyceride) export via VLDL; 2) impaired mitochondrial FA (fatty acid) oxidation (as evidenced by membrane depolarization, downregulation of Phb1 (prohibitin 1, a mitochondrial chaperone protein) and Mcj/Dnajc15 (endogenous mitochondrial repressor of respiratory chain), and accumulation of long-chain acylcarnitines); and 3) increased FA uptake. The convergence of these three factors induced TG accumulation in LD (lipid droplets). LD expansion confronts hepatocytes with a high demand of PC (phosphatidylcholine) molecules to cover the LD surface since other phospholipids, such as PE (phosphatidylethanolamine), cannot stabilize LD and prevent coalescence. In Mat1a KO this situation is aggravated, since SAMe-dependent PC synthesis via PE methylation is decreased, the PC/PE ratio reduced and mitochondrial FA oxidation impaired. To put a brake to this drain of PC molecules to LD, FA are rerouted in Mat1a KO mice liver to other catabolic (endoplasmic reticulum and peroxisome oxidation) and biosynthetic (ceramides synthesis) pathways, causing oxidative stress, inflammation and fibrosis. SAMe treatment for two months in 8-9 month old Mat1a KO mice ameliorated mitochondrial dysfunction (reduces membrane depolarization, improves Phb1 and Mcj expression, and increases SAMe transport to mitochondria) improving FA oxidation efficiency (FA and acylcarnitine levels decrease), which results in a drastic reduction in TG accumulation. SAMe treatment in Mat1a KO mice resulted in more PC available for proper membrane function, improving liver lipid homeostasis, histology (H&E, Sudan red, Sirius red) and liver injury (ALT, AST).
2017-02-02 | GSE77082 | GEO
Project description:Methionine adenosyltransferase (MAT) enzymes generate SAMe (S-adenosylmethionine), the main biological methyl donor. There are two MAT encoding genes in mammals (Mat1a and Mat2a), which show different activities and cellular distribution. Mat1a encodes the enzyme mainly expressed in normal liver. Mat1a ablation in mice results in the spontaneous development of non-alcoholic steatohepatitis (NASH). We observed that SAMe depletion in Mat1a KO mice had three main effects on hepatic lipid metabolism: 1) impaired TG (triglyceride) export via VLDL; 2) impaired mitochondrial FA (fatty acid) oxidation (as evidenced by membrane depolarization, downregulation of Phb1 (prohibitin 1, a mitochondrial chaperone protein) and Mcj/Dnajc15 (endogenous mitochondrial repressor of respiratory chain), and accumulation of long-chain acylcarnitines); and 3) increased FA uptake. The convergence of these three factors induced TG accumulation in LD (lipid droplets). LD expansion confronts hepatocytes with a high demand of PC (phosphatidylcholine) molecules to cover the LD surface since other phospholipids, such as PE (phosphatidylethanolamine), cannot stabilize LD and prevent coalescence. In Mat1a KO this situation is aggravated, since SAMe-dependent PC synthesis via PE methylation is decreased, the PC/PE ratio reduced and mitochondrial FA oxidation impaired. To put a brake to this drain of PC molecules to LD, FA are rerouted in Mat1a KO mice liver to other catabolic (endoplasmic reticulum and peroxisome oxidation) and biosynthetic (ceramides synthesis) pathways, causing oxidative stress, inflammation and fibrosis. SAMe treatment for two months in 8-9 month old Mat1a KO mice ameliorated mitochondrial dysfunction (reduces membrane depolarization, improves Phb1 and Mcj expression, and increases SAMe transport to mitochondria) improving FA oxidation efficiency (FA and acylcarnitine levels decrease), which results in a drastic reduction in TG accumulation. SAMe treatment in Mat1a KO mice resulted in more PC available for proper membrane function, improving liver lipid homeostasis, histology (H&E, Sudan red, Sirius red) and liver injury (ALT, AST).
2017-02-02 | GSE77079 | GEO
Project description:To uncover the dysregulated genes in BCa, we performed the RNA-seq to detect the gene expression levels in four BCa cells (5637, UMUC3, T24, and J82) and human immortalized urothelial cell SV-HUC-1. To search for the differentially expressed genes of for cell lines (5637, J82, UMUC3, and T24) compared to the normal cell line SV-HUC-1.
2024-04-28 | GSE231383 | GEO
Project description:To identification of key drivers involved in the development of muscle invasive bladder cancer, which displays poor prognosis, we isolated one subpopulation of human 5637 bladder cancer cells with highly invasiveness and the other subpopulation of 5637 cells with low invasiveness by Transwell method. Through proteomic analysis, differentially expressed proteins were displayed.
2018-08-27 | MSV000082854 | MassIVE
Project description:The established cell lines RT4, 5637 and T24 from human bladder TCC were obtained from the Cell Bank of the Federal University of Rio de Janeiro, Brazil. The 5637 cells harbor two TP53 mutations, at codon 72 (Arg . Pro) and codon 280 (Arg . Thr).T24 cells contain a TP53 allele encoding an in-frame deletion of tyrosine 126. Both cell lines were established from high-grade bladder tumors. No specific mutations were detected in RT4 cells, which had been established from a low-grade papillary bladder tumor. The RT4 and T24 cell lines were maintained in DulbeccoM-^Rs modified EagleM-^Rs medium (Sigma-Aldrich, Inc, St Louis, MO, USA), and the 5637 cells were kept in Roswell Park Memorial Institute medium (Sigma-Aldrich). Both media were supplemented with 10% fetal bovine serum (Cultilab Ltd, Campinas, Brazil), 100 U/mL penicillin G (Sigma-Aldrich), 100 U/mL streptomycin (Sigma-Aldrich) and 1% kanamycin sulfate (Amresco, Branded Products Group, Solon, OH, USA); cells were cultured at 37M-:C in an atmosphere of 5% CO2. A pooled reference design was chosen. More specifically, each array was hybridized with the same reference sample labeled with Cy5, while the experimental samples (control or treated) were labeled with Cy3.
2010-10-30 | E-MEXP-2859 | biostudies-arrayexpress
Project description:Mitomycin C (MMC) is the gold standard treatment for non-muscle invasive bladder cancer (NMIBC). We aimed to evaluate in bladder cancer cell lines (T24, 5637, TCC-SUP and CLS-439) the transcriptomic response to MMC treatment. We used Gene Set Enrichment Analysis (GSEA) to identify biological processes and pathways modulated by MMC treatment.
2021-01-02 | GSE151505 | GEO