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Expression profiling in RCC4/VHL cells under HIF and AHR co-activating conditions

ABSTRACT: Expression profiling in RCC4/VHL cells under HIF and AHR co-activating conditions

PROVIDER: PRJNA848810 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19639069_1.fastq.gz	Fastqsanger.gz
	SRR19639069_2.fastq.gz	Fastqsanger.gz
	SRR19639070_1.fastq.gz	Fastqsanger.gz
	SRR19639070_2.fastq.gz	Fastqsanger.gz
	SRR19639071_1.fastq.gz	Fastqsanger.gz

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RCC4/VHL cells under HIF and AHR co-activating conditions

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Genome binding/occupancy profiling of HIF and AHR in RCC4 cells under co-activating conditions

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Genome binding/occupancy profiling of HIF and AHR in RCC4 cells under co-activating conditions

Project description:Genome binding/occupancy profiling of HIF and AHR in RCC4 cells under co-activating conditions

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RCC4/VHL cells under HIF and AHR co-activating conditions

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-01-24 | GSE206029 | GEO

Gene expression analysis in primary human renal tumors, categorized by VHL genotype and HIF-alpha expression

Project description:Human renal cell carcinomas (RCC) have differential expression of HIF-1alpha and HIF-2alpha, depending on VHL genotype and other events. Here, we have divided a series of RCC samples for HIF-alpha expression and VHL genotype, in order to define differentially expressed genes Keywords: Patient Sample Study A total of 57 frozen RCC samples were stained for HIF-1alpha and HIF-2alpha, and genotyped for VHL. 5 VHL WT/HIF-negative, 8 VHL-deficient/HIF-1alpha+/HIF-2alpha+ and 8 VHL-deficient/HIF-2alpha+ tumors were selected for microarray

2008-12-27 | E-GEOD-11904 | biostudies-arrayexpress

Transcription profiling of HIF dependent and independent effects of VHL inactivation in C. elegans

Project description:The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function.

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Array CGH analysis in primary human renal tumors, categorized by VHL genotype and HIF-alpha expression

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Epigenetic expansion of VHL-HIF signal output drives multiorgan metastasis in renal cancer

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. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.

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