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Exometabolomics of HK2, 786-O cells cultured in Plasmax media

ABSTRACT: The objective of this study is to analyse the exometabolomics of human epithelial renal cell line HK2 and clear cell renal cell carcinoma (ccRCC) cell lines 786-O, 786-M1A, 786-M2A, OS-RC-2, OS-LM1 and RFX-631 that are cultured with the Plasmax media. This is part 3 of the study, and the experimental number is MS51.

ORGANISM(S): Human Homo Sapiens

TISSUE(S): Cultured Cells

DISEASE(S): Cancer

SUBMITTER: Ming Yang

PROVIDER: ST002226 | MetabolomicsWorkbench | Fri Jul 15 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

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Intracellular metabolic profile of renal cells cultured in Plasmax

Project description:The objective of this experiment is to analyse the metabolic profiles of human renal epithelial cells HK2 and ccRCC cell lines 786-O, 786-M1A and 786-M2A in Plasmax media. The experiment was conducted on three different days using cells with different passage numbers. This is Part 5 of a study and the experimental number is MS55.

2022-07-15 | ST002224 | MetabolomicsWorkbench

Assessing the contribution of branched-chain amino acid (BCAA)-derived nitrogen to amino acid biosynthesis in renal cell lines HK2 and 786-O.

Project description:The objective of this experiment is to test the contribution of branched-chain amino acids (BCAA)-derived nitrogen to the generation of de novo amino acids in renal cells through transamination reactions. To test this hypothesis, we incubated human renal epithelial cell line HK2 and ccRCC cell lines 786-O, 786-M1A and 786-M2A with 15N-leucine and 15N-isoleucine in Plasmax media for 27h. Data were generated from 5 independent cultures. This is Part 2 of the study and the experimental number is MS48.

2022-07-15 | ST002227 | MetabolomicsWorkbench

Catabolism of branched-chain amino acids (BCAAs) in renal cells HK2 and 786-O

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2022-07-15 | ST002220 | MetabolomicsWorkbench

Glutaminolysis contribution to the carbon backbone of aspartate and glutamate in ccRCC

Project description:The objective of this experiment is to test the contribution of the carbons derived from glutamine to the generation of aspartate and glutamate in human epithelial renal cells HK2 and ccRCC cell lines 786-O and 786-M1A. To test this hypothesis, we incubated all cells with 13C5-glutamine in Plasmax media with or without a pharmacological inhibitor of glutaminase CB-839. This is Part 7 of a study and the experimental number is MS57.

2022-07-15 | ST002222 | MetabolomicsWorkbench

Glutaminolysis contribution to the carbon backbone of aspartate through ATP Citrate Lyase (ACLY) in ccRCC

Project description:The objective of this experiment is to test the contribution of the carbons from glutamine to generation of aspartate via ATP citrate lyase (ACLY) in human epithelial renal cells HK2 and ccRCC cell lines 786-O and 786-M1A. To test this hypothesis, we incubated all cells with 13C5-glutamine in Plasmax media with or without a pharmacological inhibitor of ACLY. This is Part 8 of the study and the experimental number is MS58.

2022-07-15 | ST002221 | MetabolomicsWorkbench

Time sensitive contribution of the BCAA catabolism to the TCA cycle carbons in HK2, 786-O, OS-RC-2 and RFX-631

Project description:The objective of this experiment is to test the contribution of the branched chain amino acids catabolism to the carbons used in the TCA cycle. To test this hypothesis, we incubated human renal epithelial cells (HK2) and ccRCC cell lines (786-O, 786-M1A, OS-RC-2, OS-LM1, RFX-631) with 13C6-leucine and 13C6-isoleucine in Plasmax media for 10 mins, 1 hour and 3 hours. Data were generated from 5 independent cultures. This is Part 4 of the study and the experiment number is MS52.

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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

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

Systematic Analysis of Transcriptomic Profile of Renal Cell Carcinoma under Long-Term Hypoxia using Next-Generation Sequencing and Bioinformatics

Project description:Patients with clear cell renal cell carcinoma (ccRCC) are often diagnosed with both von Hippel-Lindau (VHL) mutations and the constitutive activation of hypoxia-inducible factor-dependent signaling. In this study, we investigated the effects of long-term hypoxia in 786-O, a VHL-defective renal cell carcinoma cell line, to identify potential genes and microRNAs associated with tumor malignancy. The transcriptomic profiles of 786-O under normoxia, short-term hypoxia, and long-term hypoxia were analyzed using next-generation sequencing. The results showed that long-term hypoxia promoted the ability of colony formation and transwell migration compared to normoxia. In addition, the differentially expressed genes induced by long-term hypoxia were involved in various biological processes including cell proliferation, the tumor necrosis factor signaling pathway, basal cell carcinoma, and cancer pathways. The upregulated (L1CAM and FBN1) and downregulated (AUTS2, MAPT, AGT, and USH1C) genes in 786-O under long-term hypoxia were also observed in clinical ccRCC samples along with malignant grade. The expressions of these genes were significantly correlated with survival outcomes in patients with renal cancer. We also found that long-term hypoxia in 786-O resulted in decreased expressions of hsa-miR-100 and has-miR-378, and this effect was also observed in samples of metastatic ccRCC compared to samples of non-metastatic ccRCC. These findings may provide a new direction for the study of potential molecular mechanisms associated with the progression of ccRCC.

2017-12-12 | GSE107848 | GEO

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Project description:We aim to the investigate the role of MST1/2 inhibitor XMU-MP-1 in kindy renal clear cell carcinoma (ccRCC) progression. 786-O cells were used as the model.

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