Transcriptome profiling of 786-O RCC cells transduced with control vector or PRDM16 lentivirus.
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ABSTRACT:
PROVIDER: PRJNA533637 | ENA |
REPOSITORIES: ENA
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Project description:Recent large-scale data sets indicate the emerging importance of alterations of the epigenome in renal cell carcinoma (RCC). Analysis of transcriptomic data of patient samples including normal kidney, primary tumor, and metastatic tumor deposits demonstrates epigenetic silencing of the gene encoding the transcription factor PR domain-containing 16 (PRDM16). PRDM16 has a prominent role in adipocyte metabolism but is also highly expressed in the kidney. The role of PRDM16 in renal cancer has not been investigated. RNAseq analysis reveals that PRDM16 imparts a predominantly repressive effect on the RCC transcriptome including suppression of SEMA5B (semaphorin 5B), a target gene of hypoxia inducible factor (HIF). Collectively, our data uncover a novel epigenetic basis by which HIF target gene expression is amplified in kidney cancer. Moreover, they demonstrate a new mechanism by which PRDM16 exerts its tumor suppressive effects.
2020-03-20 | GSE130049 | GEO
Project description:PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16. undifferentiated C2C12 myoblasts were stably expressed with retroviral PRDM16 or vector control. Total RNAs were isolated by Trizol, and subjected to Affymetrix microarrays.
2010-03-03 | E-GEOD-15895 | biostudies-arrayexpress
Project description:PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16.
2009-07-31 | GSE15895 | GEO
Project description:While early stages of clear cell renal cell carcinoma (ccRCC) are curable, survival outcome for metastatic ccRCC remains poor. The purpose of the current study was to apply a new individualized bioinformatics analysis (IBA) strategy to these transcriptome data in conjunction with Gene Set Enrichment Analysis of the Connectivity Map (C-MAP) database to identify and reposition FDA-approved drugs for anti-cancer therapy. We demonstrated that one of the drugs predicted to revert the RCC gene signature towards normal kidney, pentamidine, is effective against RCC cells in culture and in a RCC xenograft model. Most importantly, pentamidine slows tumor growth in the 786-O human ccRCC xenograft mouse model. To determine which genes are regulated by pentamidine in a human RCC cell line, 786-O, we treated these cells with pentamidine and performed transcriptional profiling analysis. We used microarrays to determine the set of genes regulated by pentamidine in 786-O renal cell cancer cells. Total RNA was isolated from 786-O cells treated with 25 μM pentamidine or vehicle control (DMSO) for 6 hours and hybridized to Affymetrix microarrays.
2014-08-05 | E-GEOD-54709 | biostudies-arrayexpress
Project description:While early stages of clear cell renal cell carcinoma (ccRCC) are curable, survival outcome for metastatic ccRCC remains poor. The purpose of the current study was to apply a new individualized bioinformatics analysis (IBA) strategy to these transcriptome data in conjunction with Gene Set Enrichment Analysis of the Connectivity Map (C-MAP) database to identify and reposition FDA-approved drugs for anti-cancer therapy. We demonstrated that one of the drugs predicted to revert the RCC gene signature towards normal kidney, pentamidine, is effective against RCC cells in culture and in a RCC xenograft model. Most importantly, pentamidine slows tumor growth in the 786-O human ccRCC xenograft mouse model. To determine which genes are regulated by pentamidine in a human RCC cell line, 786-O, we treated these cells with pentamidine and performed transcriptional profiling analysis. We used microarrays to determine the set of genes regulated by pentamidine in 786-O renal cell cancer cells.
2014-08-05 | GSE54709 | GEO
Project description:RCC cells (786-O) were transfected with VHL. The parental cell line should be compared to the transfectant (+ VHL) under nomoxia as well as under hypoxia conditions. We want to distinct the VHL-mediated gene expression from the hypoxia-mediated and study the influence of both on the cellular metabolism. RNA of VHL-negative 786-O RCC cell line and VHL-transfectants incubated during normoxia and hypoxia conditions were analysed by cDNA microarray.
2015-01-22 | E-GEOD-65168 | biostudies-arrayexpress
Project description:Genome-wide DNA methylation profiling of 786-0 RCC cells treated with decitabine (100nM and 300nM) or DMSO vehicle. The Illumina Infinium HumanMethylation EPIC BeadChip was used to obtain DNA methylation profiles across approximately 850K CpGs.
2020-06-01 | GSE146179 | GEO
Project description:RCC cells (786-O) were transfected with VHL. The parental cell line should be compared to the transfectant (+ VHL) under nomoxia as well as under hypoxia conditions. We want to distinct the VHL-mediated gene expression from the hypoxia-mediated and study the influence of both on the cellular metabolism.
2015-01-22 | GSE65168 | GEO
Project description:RCC cell lines (786-O cell line and Caki-1 cell line)were co-cultured with human renal glomerular endothelial cells (HGECs) treated with si-RNA of INSR (HGEC-siINSR). Gene expression alteration was analyzed using microarray.
2023-04-27 | GSE230698 | GEO
Project description:786-0 is a cell line derived from a clear cell renal carcinoma. Previous studies have shown that the 786-O cell line harbors an inactivating mutation in the von-Hippel Lindau (VHL) gene. Mutations in the VHL gene occur in the majority of sporadic clear cell renal cell. To determine how inactivation of the VHL affects cellular functions, we created a derivative of 786-0, which we call 786-VHL in which a functional allele of VHL has been introduced back into the 786-O cell line.
2010-06-10 | GSE22256 | GEO