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Microarray analysis of gene expression after suppression of PBRM1 or KDM5C in 786-O VHL+/+ or VHL-/- cells

ABSTRACT: Microarray analysis of gene expression after suppression of PBRM1 or KDM5C in 786-O VHL+/+ or VHL-/- cells

PROVIDER: PRJNA422885 | ENA |

REPOSITORIES: ENA

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Microarray analysis of gene expression after suppression of PBRM1 or KDM5C in 786-O VHL+/+ or VHL-/- cells

Project description:1. PBRM1 loss elicited very similar transcriptional changes as KDM5C loss; 2. PBRM1 loss, and to a lesser extent KDM5C loss, elicited greater transcriptional response in VHL-/- cells than that in VHL+/+ cells.

2018-11-05 | GSE108229 | GEO

786-O and 786-VHL in EMCV study

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. The renal cell carcinoma cell line 786-0, which harbors a mutated allele of VHL, was compared to a cell line derived from 786-0, termed 786-VHL, that contains a functional allele of VHL. Genes whose expression characteristics were dependent on functional VHL were identified.

2010-06-23 | E-GEOD-22256 | biostudies-arrayexpress

786-O and 786-VHL in EMCV study

2010-06-10 | GSE22256 | GEO

RNA-seq of a VHL-/- human renal cancer cell line 786-0 transfected with 3 vectors

Project description:The human renal cancer cell line 786-0 was transfected with 3 vectors allowing the doxycycline-inducible expression of 1) the full length wild type sequence of VHL: 786-0 VHL WT, VHL+/+, 2) the R167Q mutant : 786-0 R167Q, VHL mutated, 3) the empty vector : 786-0 EV, VHL-/-. The aim of the study was to examine whether the VHL-R167Q mutation, which is associated with a high risk of developping clear cell renal carcinomas, could impact the plasticity of renal carcinoma cells.

2021-12-09 | E-MTAB-11168 | biostudies-arrayexpress

Next Generation Sequencing of 786-O-Ctrl and786-O-VHL Transcriptomes

Project description:Inactivation of the E3 ubiquitin ligase protein von Hippel-Lindau (VHL) is critical to clear cell renal cell carcinomas (ccRCC) and VHL syndrome. VHL loss leads to stabilization of hypoxia-inducible factor α (HIFα) and other substrate proteins, which may drive various tumor-promoting pathways. This process is likely reversible, because even in the highly aggressive human VHL-deficient ccRCC cell line 786-O, restoring VHL expression almost completely abolishes orthotopic tumor formation in immuno-deficient mice. This result highlights the potential of treating ccRCC by re-expressing VHL with gene therapy. However, there is inadequate understanding of the consequence of VHL restoration at the molecular level. Here, we reinstalled VHL expression in 786-O and performed transcriptome, proteome and ubiquitome profiling to assess the molecular impact.

2021-10-18 | GSE186013 | GEO

Identification of transcriptional changes upon genetic deletion of Vhl, Pbrm1 and double deletion of both Vhl and Pbrm1

Project description:To determine why double deficiency of Vhl and Pbrm1 but not single deficiency of either gene resulted in ccRCC, we performed gene expression profiling of RNA isolated from renal cortices of 3-month-old WT, VhlF/FKsp-Cre, Pbrm1F/FKsp-Cre, and VhlF/FPbrm1F/FKsp-Cre mice.

2017-03-06 | GSE83597 | GEO

Vhl and Pbrm1 double deletion effect on kidney

Project description:Vhl and Pbrm1 double deletion effect on kidney

| PRJNA326726 | ENA

Gene expression changes in response to VHL-reintroduction in metastatic 786-M1A cells.

Project description:Inactivation of the von Hippel-Lindau tumor suppressor gene, VHL, is an archetypical tumor-initiating event in clear cell renal carcinoma (ccRCC) that leads to the activation of hypoxia-inducible transcription factors (HIFs). However, VHL mutation status in ccRCC is not correlated with clinical outcome. Here we show that during ccRCC progression, cancer cells exploit diverse epigenetic alterations to empower a branch of the VHL-HIF pathway for metastasis, and the strength of this activation is associated with poor clinical outcome. By analyzing metastatic subpopulations of VHL-deficient ccRCC cells, we discovered an epigenetically altered VHL-HIF response that is specific to metastatic ccRCC. Focusing on the two most prominent pro-metastatic VHL-HIF target genes, we show that loss of polycomb repressive complex 2 (PRC2)-dependent histone H3 Lys27 trimethylation (H3K27me3) activates HIF-driven chemokine (C-X-C motif) receptor 4 (CXCR4) expression in support of chemotactic cell invasion, whereas loss of DNA methylation enables HIF-driven cytohesin 1 interacting protein (CYTIP) expression to protect cancer cells from death cytokine signals. Thus, metastasis in ccRCC is based on an epigenetically expanded output of the tumor-initiating pathway. Gene expression data from metastatic 786-M1A cells with and without reintroduced HA-VHL. The empty vector, pBabe-puro, was used as control.

2012-12-05 | E-GEOD-32297 | biostudies-arrayexpress

VHL/HIF2a axis alters transcriptomic profiles in ccRCC

Project description:VHL loss is the most common genetic alteration event in ccRCC. VHL loss stabilizes hypoxia-inducible factor-2 alpha (HIF2a). We compared the changes in transcriptomics profiles after VHL restoration or HIF2a siRNA knockdown in 786-O cells.

2017-08-22 | GSE102097 | GEO

VHL restoration alters cis-regulatory landscape

Project description:VHL loss is the most common genetic alteration event in ccRCC. By profiling histone modifications from VHL-deficient ccRCC primary tumors and cell lines, we identifed tumor-associated promoters and enhancers. We next investigate whether VHL restoration alters tumor associated promoters and enhancers. We compared H3K27ac ChIP-seq with and without VHL restoration in 786-O cells. Restoration of wild-type VHL significantly altered a subset of tumor enhancers but affected promoters to a less extent.

2017-08-22 | GSE102095 | GEO

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