Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA156303 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE34979: Array-based CGH analysis of ccRCC derived cell lines GSE34981: miRNA transcript levels in ccRCC-derived cell lines and proximal tubular epithelial cell samples Refer to individual Series
2012-11-01 | E-GEOD-34985 | biostudies-arrayexpress
Project description:Despite numerous studies reporting deregulated microRNA (miRNA) and gene expression patterns in clear cell renal cell carcinoma (ccRCC), no direct comparisons have been made to its presumed normal counterpart; the renal proximal epithelial tubular cells (PTEC). The aim of this study was to determine the miRNA expression profiles of ten clear cell renal cell carcinoma-derived cell lines and short-term cultures of PTEC, and to correlate these with their gene expression, and copy-number profiles. Using microarray-based methods, a significantly altered expression level in ccRCC cell lines was observed for 23 miRNAs and 1630 genes. The set of miRNAs with significantly decreased expression levels include all members of the miR-200 family known to be involved in the epithelial to mesenchymal transition (EMT) process. Expression levels of 13 of the 47 validated target genes for the downregulated miRNAs were increased more than two-fold. Our data reinforce the importance of the EMT process in the development of ccRCC. For mRNA expression data of these cell lines see GEO Series accession number GSE20491. MicroRNA profiling was performed on two proximal tubular epithelial cell samples (both cell samples were hybridized twice (biological duplicates)) and ten clear cell renal cell carcinoma- derived cell lines (one of which; RCC-JF in duplicate)
2012-11-01 | E-GEOD-34981 | biostudies-arrayexpress
Project description:Despite numerous studies reporting deregulated microRNA (miRNA) and gene expression patterns in clear cell renal cell carcinoma (ccRCC), no direct comparisons have been made to its presumed normal counterpart; the renal proximal epithelial tubular cells (PTEC). The aim of this study was to determine the miRNA expression profiles of ten clear cell renal cell carcinoma-derived cell lines and short-term cultures of PTEC, and to correlate these with their gene expression, and copy-number profiles. Using microarray-based methods, a significantly altered expression level in ccRCC cell lines was observed for 23 miRNAs and 1630 genes. The set of miRNAs with significantly decreased expression levels include all members of the miR-200 family known to be involved in the epithelial to mesenchymal transition (EMT) process. Expression levels of 13 of the 47 validated target genes for the downregulated miRNAs were increased more than two-fold. Our data reinforce the importance of the EMT process in the development of ccRCC. For mRNA expression data of these cell lines see GEO Series accession number GSE20491.
2012-11-01 | GSE34981 | GEO
Project description:Clear cell renal cell carcinomas (ccRCC) are characterized by arm-wide chromosomal alterations. Loss at 14q is associated with disease aggressiveness in ccRCC, which responds poorly to chemotherapeutics. The 14q locus contains one of the largest miRNA clusters in the human genome; however, little is known about the contribution of these miRNAs to ccRCC pathogenesis. In this regard, we investigated the expression pattern of selected miRNAs at the 14q32 locus in TCGA kidney tumors and in ccRCC cell lines. We validated that the miRNA cluster is downregulated in ccRCC (and cell lines) as well as in papillary kidney tumors relative to normal kidney tissues and primary renal proximal tubule epithelial (RPTEC) cells. We demonstrated that agents modulating expression of DNMT1 (e.g., 5-Aza-deoxycytidine) could modulate miRNA expression in ccRCC cell lines. Lysophosphatidic acid (LPA, a Lysophospholipid mediator elevated in ccRCC) not only increased labile iron content but also modulated expression of 14q32 miRNAs. Through an overexpression approach targeting a subset of 14q32 miRNAs (specifically at subcluster A: miR-431, miR-432, miR-127, and miR-433) in 769-P cells, we uncovered changes in cellular viability and claudin-1, a tight junction marker. A global proteomic approach was implemented using these miRNA overexpressing cell lines which uncovered ATXN2 as a highly downregulated target, which has a role in chronic kidney disease pathogenesis. Collectively, these findings support a contribution of miRNAs at 14q32 in ccRCC pathogenesis.
2023-05-10 | PXD036428 | Pride
Project description:Diabetic kidney disease is a major complication in diabetes mellitus, and the most common reason for end-stage renal disease. Patients suffering from diabetes mellitus encounter glomerular damage by basement membrane thickening, and develop albuminuria. Subsequently, albuminuria can deteriorate the tubular function and impair the renal outcome. The impact of diabetic stress conditions on the metabolome was investigated by untargeted gas chromatography-mass spectrometry (GC-MS) analyses. The results were validated by qPCR analyses. In total, four cell lines were tested, representing the glomerulus, proximal nephron tubule, and collecting duct. Both murine and human cell lines were used. In podocytes, proximal tubular and collecting duct cells, high glucose concentrations led to global metabolic alterations in amino acid metabolism and the polyol pathway. Albumin overload led to the further activation of the latter pathway in human proximal tubular cells. In the proximal tubular cells, aldo-keto reductase was concordantly increased by glucose, and partially increased by albumin overload. Here, the combinatorial impact of two stressful agents in diabetes on the metabolome of kidney cells was investigated, revealing effects of glucose and albumin on polyol metabolism in human proximal tubular cells. This study shows the importance of including highly concentrated albumin in in vitro studies for mimicking diabetic kidney disease.
2019-10-08 | MTBLS1093 | MetaboLights
Project description:Even though mutations in epigenetic regulators have been seen in renal neoplasms, their effects on the epigenome have not been elucidated. High resolution analysis of DNA methylation was performed in clear cell RCCs and matched microdissected renal tubular controls and revealed widespread hypermethylation that preferentially affected gene bodies and CpG shores. Aberrant methylation was particularly enriched in kidney specific enhancer regions associated with H3K4Me1 marks. MOTIF analysis of aberrantly methylated loci revealed enrichment for AHR, HAIRY and HIF-1 transcription factors, reflecting dysregulated hypoxia and NOTCH pathways in RCC. Parallel copy number analysis demonstrated that both genetic and epigenetic alterations led to NOTCH pathway activation in RCC. NOTCH ligands,JAGGED1 and JAGGED2, were overexpressed and associated with hypomethylation and amplification respectively in RCC samples. Examination of TCGA RNA-seq dataset revealed widespread activation of NOTCH pathway in 405 RCC samples. Samples with NOTCH pathway activation were also clinically distinct and were associated with better overall survival. Finally, transgenic expression of NOTCH1 led to dysplastic hyperproliferation of tubular epithelial cells in vivo confirming the procarcinogenic role of NOTCH. In summary, our study is the first global methylome analysis of RCC and reveals that mechanistic basis of NOTCH pathway activation in RCC. We analyzed the methylome of clear cell renal cell cancer (CCRCC) by the HELP assay. 13 cases of histologically verified CCRCC tumor samples were compared to 13 control microdissected proximal tubules from non-tumor part of nephrectomy samples
2014-07-31 | E-GEOD-49420 | biostudies-arrayexpress
Project description:We show that in an appropriate feeder cell-based culture system, it is feasible to isolate and long-term expand the progenitor-like SOX9+ renal epithelial cells (SOX9+ RECs) from adult mammalians. Single cell-derived SOX9+ REC lines can be established from human needle biopsy or urine samples with molecular homogeneity and genomic stability maintained during culture. Such cells grown in 3D culture system could self-organize into renal organoids composed of proximal tubular, Loop of Henle (LOH) and distal tubular cells as illustrated by single cell transcriptomic analysis.
2022-04-22 | GSE143154 | GEO
Project description:While analyzing mRNA expression profiles of clear cell renal cell carcinoma (ccRCC) tumors, we found that the mRNAs that are bound at their 3' UTRs by muscleblind-like splicing regulator 2 (Mbnl2) and epithelial splicing regulatory protein 2 (ESRP2) are up-regulated in tumor compared to patient-matched normal tissues. Given that MBNL2 increases the stability of its targets and ESRP2 destabilizes its targets, we predicted that, in ccRCC tumors, MBNL2 activity increases, while ESRP2 activity decreases. To investigate the effect of each of these two RNA-binding proteins (RBPs) on the transcriptome of the cell, we used shRNA to knockdown MBNL2 in two different cell line models of ccRCC (786-O and A-498), and also to knockdown ESRP2 in normal primary renal proximal tubule epithelial cells (PRPTEC). RNA-seq revealed that MBNL2 knockdown partially reverses the ccRCC-associated transcriptome in ccRCC cell lines, whereas ESRP2 knockdown shifts the transcriptome of PRPTEC toward that of ccRCC.
2018-03-23 | GSE83999 | GEO
Project description:proximal tubular epithelial cell apoptosis were incubated with 5% plasma of septic patients or healthy volunteers diluited in RPMI 1640
2008-03-15 | E-MEXP-1510 | biostudies-arrayexpress
Project description:Purpose: The aim of the present study was to identify and characterize in tissue samples of clear cell-renal cell carcinoma (ccRCC) a population of CD133+/CD24+ cancer cells (RCC-derived cells-RDCs) and to study the differences with their nonneoplastic counterpart, tubular Adult Renal Progenitor Cells (ARPCs). Materials and methods: CD133+/CD24+ RDCs were isolated from 40 patients. The mesenchymal phenotype and stemness proteomic profile of these RDCs were characterized. The colony-forming efficiency and self-renewal ability were tested with limiting dilution. The tumorigenic properties were evaluated in vitro with Soft Agar Assay. The angiogenic response was evaluated in vivo with the chorioallantoic membrane angiogenic assay. Microarray analysis was performed on 6 tARPCs and 6 RDCs clones. Expression of membrane proteins was evaluated with flowcytometry and immunofluorescence staining. Results: CD133+/CD24+ cells were isolated from normal and tumoral kidney tissue. FACS analysis showed that RDCs did not express the mesenchymal stem cell markers. We showed that CD133+/CD24+ tumor cells were more undifferentiated than tARPCs. RDCs were clonigenic and able to differentiate into adipocytes, epithelial and osteogenic cells. RDCs were able to regenerate tumor cells in vitro and to induce angiogenesis in vivo. The gene expression profile identified CTR2 as a membrane marker for this neoplastic population. Conclusions: Our results indicate the presence, in ccRCC, of a CD133+/CD24+/CTR2+ cancer cells population. These cells possess some stem cell-like features, including in vitro self-maintenance and differentiating capabilities, and are able to induce an angiogenic response in vivo. Study of gene expression profiling of Renal Cancer Cells (RCSCs), tubular Adult Renal Progenitor Cells (tARPCs), Renal Proximal Tubular Cells (RPTEC) and Mesenchymal Stem Cells (MSC). To highlight the similarities and the differences with known renal stem populations and with terminally differentiated renal cells, for each patient, 6 subcultures of tubular ARPCs (tARPCs), 3 subcultures of the MSC and 3 subcultures of the RPTEC were included in the analysis.
2015-12-15 | E-GEOD-48550 | biostudies-arrayexpress