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Intracellular metabolic profile of renal cells cultured in Plasmax

ABSTRACT: 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.

ORGANISM(S): Human Homo Sapiens

TISSUE(S): Cultured Cells

DISEASE(S): Cancer

SUBMITTER: Ming Yang

PROVIDER: ST002224 | MetabolomicsWorkbench | Fri Jul 15 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

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

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

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

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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.

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