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Effects of depletion of EPAS1 and knocking down TNFSF10 in 786-O cell lines.

ABSTRACT: VHL loss leads to the stabilization of hypoxia-inducible factor α (HIFα), which may drive various tumor-promoting pathways. Here, we depletion expression of HIF2α in 786-O and performed transcriptome profiling to assess the molecular impact. TRAIL represents a promising avenue for cancer therapy due to its ability to selectively target and kill tumor cells. However, its effectiveness is variable across different cancer types, even with some tumors exhibiting high levels of TRAIL expression. To investigate this situation, we used shRNA to target TNFSF10, aiming to understand its impact on tumor development.

ORGANISM(S): Homo sapiens

PROVIDER: GSE259401 | GEO | 2024/03/08

REPOSITORIES: GEO

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Effects of depletion of EPAS1 and knocking down TNFSF10 in 786-O cell lines.

Project description:Effects of depletion of EPAS1 and knocking down TNFSF10 in 786-O cell lines.

| PRJNA1081410 | ENA

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

Transcription factors enriched in tumor-associated enhancers in VHL-deficient ccRCC

Project description:VHL loss is the most common genetic alteration event in ccRCC. We profiled histone modifications from VHL-deficient ccRCC primary tumors and cell lines. We show that ccRCCs exhibit a pervasive gain of enhancers around hypoxic and metabolic transcriptional targets. Motif analysis using HOMER revealed significant enrichment of AP-1, ETS, NFĸB and HIFα in tumor enhancers. We generated ChIP-seq binding data for c-Jun, ETS1, NFĸB, and P300, a histone acetyltransferase, in 786-O cells. ChIP-seq profiles of HIF2α and HIF1β in 786-O were already generated previously (GSE34871)

2017-08-22 | GSE86092 | GEO

Tenascin-C shapes TRAIL control over tumor immunity

Project description:TRAIL cytotoxicity is exploited as anti-cancer therapy since many years, however incomplete knowledge is generating many obstacles. Here, we address whether the highly abundant extracellular matrix molecule tenascin-C (TNC) orchestrating an immune suppressive tumor microenvironment and binding TRAIL impacts TRAIL cytotoxicity. We used an immune competent autologous NT193 breast cancer model with a knockdown (KD) of Tnfsf10 (encoding TRAIL) and observed accelerated tumor growth marked by less apoptosis, more proliferation and less myeloid cell infiltration as seen by flow cytometry. Grafting the same Tnfsf10 KD cells into a TNC knockout host showed repressed tumor growth suggesting that TNC is involved in regulating TRAIL functions.

2024-05-30 | E-MTAB-14089 | biostudies-arrayexpress

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

Genome-wide chromatin profiles of ZNF395 [RNA-seq]

Project description:Hypoxia signaling induced by VHL deficiency fuels growth but also poses immense metabolic stress to clear cell renal cell carcinomas (ccRCCs). Tumor cells depend on glutamine as the primary source of tricarboxylic acid (TCA) anaplerosis. Hypoxia-inducible factor alpha (HIFα) governs glycolysis but does not directly regulate glutamine metabolism; instead, the factor responsible for orchestrating glutamine metabolism and mitochondrial adaptations to hypoxia remains elusive. We now show that ZNF395 is a hypoxia-responsive factor that regulates glutamine metabolism in the mitochondria. ZNF395 is activated by a HIF2α-modulated super-enhancer but plays non-redundant functions from HIF2α. Specifically, ZNF395 facilitates the transcription of enzymes essential for glutaminolysis, including glutaminase (GLS) and isocitrate dehydrogenase 2 (IDH2). Functionally, ZNF395 depletion results in reduced TCA intermediates and their derivatives, including amino acids, glutathione and pyrimidine nucleotides. In addition, ZNF395 depletion diminishes mitochondrial respiration; restoration of complex I function rescues the effects of ZNF395 depletion. Our study underscores the coordinated role of HIFα and ZNF395 in shaping metabolic adaptations in response to hypoxia in VHL-deficient ccRCCs.

2024-10-01 | GSE247117 | GEO

Genome-wide chromatin profiles of ZNF395 [ChIP-seq]

2024-10-01 | GSE247116 | GEO

Expression data from 786-O renal cell cancer cells treated with pentamidine

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 Î¼M pentamidine or vehicle control (DMSO) for 6 hours and hybridized to Affymetrix microarrays.

2014-08-05 | E-GEOD-54709 | biostudies-arrayexpress

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