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An Integrated Metabolic Atlas of Clear Cell Renal Cell Carcinoma

ABSTRACT: Changes in cellular metabolism contribute to the development and progression of tumors, and can render tumors vulnerable to interventions. However, studies of human cancer metabolism remain limited due to technical challenges of detecting and quantifying small molecules, the highly interconnected nature of metabolic pathways, and the lack of designated tools to analyze and integrate metabolomics with other –omics data. Our study generates the largest comprehensive metabolomics dataset on a single cancer type, and provides a significant advance in integration of metabolomics with sequencing data. Our results highlight the massive re-organization of cellular metabolism as tumors progress and acquire more aggressive features. The results of our work are made available through an interactive public data portal for cancer research community.

ORGANISM(S): Homo sapiens

PROVIDER: GSE74734 | GEO | 2016/03/08

SECONDARY ACCESSION(S): PRJNA301435

REPOSITORIES: GEO

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An Integrated Metabolic Atlas of Clear Cell Renal Cell Carcinoma

Project description:Changes in cellular metabolism contribute to the development and progression of tumors, and can render tumors vulnerable to interventions. However, studies of human cancer metabolism remain limited due to technical challenges of detecting and quantifying small molecules, the highly interconnected nature of metabolic pathways, and the lack of designated tools to analyze and integrate metabolomics with other âomics data. Our study generates the largest comprehensive metabolomics dataset on a single cancer type, and provides a significant advance in integration of metabolomics with sequencing data. Our results highlight the massive re-organization of cellular metabolism as tumors progress and acquire more aggressive features. The results of our work are made available through an interactive public data portal for cancer research community. 10 RNA samples from human ccRCC tumors analyzed from the high glutathione cluster

2016-03-08 | E-GEOD-74734 | biostudies-arrayexpress

Patient-Derived Orthotopic Xenografts and Cell Lines from Pediatric High-Grade Glioma Recapitulate Heterogeneity of Histopathology, Molecular Signatures and Drug Response

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GPX8 regulates clear cell renal cell carcinoma tumorigenesis through promoting lipogenesis by NNMT

Project description:By analyzing RNAseq data from TCGA in ccRCC and metabolomics data from CCLE, we identified the strong correlation of GPX8 with the lipid and glycogen metabolism, which are highly upregulated in ccRCC. We validated this observation by knocking out GPX8 in Caki1 (ccRCC cell line). Using transcript profiling, we confirmed the association of GPX8 with de novo lipogenesis and suppressed fatty acid oxidation. Mechanically, from RNA-seq data we also found the decrease of NNMT upon GPX8 KO, which functions as the downstream of GPX8 and regulates the lipid phenotype in ccRCC.

2022-08-01 | GSE193249 | GEO

PD-L1 mediates IFNγ-regulation of glucose but not of tryptophan metabolism in clear cell renal cell carcinoma

Project description:The immune checkpoint programmed death-ligand 1 (PD-L1) is expressed on the cell surface of tumor cells and is key for maintaining an immunosuppressive microenvironment through its interaction with the programmed death 1 (PD-1). Clear cell renal cell carcinoma (ccRCC) is a highly immunogenic cancer characterized by an aberrant aerobic glycolytic metabolism and is known to overexpress PD-L1. Multiple immunotherapies have been approved for the treatment of ccRCC, including cytokines and immune checkpoint inhibitors. Recently the intrinsic role of PD-L1 and interferon gamma (IFNγ) signaling have been studied in several types of tumor cells, yet it remains unclear how they affect the metabolism and signaling pathways of ccRCC. Using metabolomics, metabolic assays and RNAseq, we showed that IFNγ enhanced aerobic glycolysis and tryptophan metabolism in ccRCC cells in vitro and induced the transcriptional expression of signaling pathways related to inflammation, cell proliferation and cellular energetics. These metabolic and transcriptional effects were partially reversed following transient PD-L1 silencing. Aerobic glycolysis, as well as signaling pathways related to inflammation, were not induced by IFNγ when PD-L1 was silenced, however, tryptophan metabolism and activation of Jak2 and STAT1 were maintained. Our data demonstrate that PD-L1 expression is required to mediate some of IFNγ’s effect in ccRCC cells and highlight the importance of PD-L1 signaling in regulating the metabolism of ccRCC cells in response to inflammatory signals.

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quanTIseq: quantifying immune contexture of human tumors

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Project description:Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, and it has a 5-year survival rate of 85% for European children. But for subsets of patients who fail to respond to standard of care chemotherapeutics, treatment options are limited, and clinical prognosis is poor. To establish a platform and methodology to better characterize ALL subtypes and identify their pharmacologic vulnerabilities, we assembled a biobank of 49 readily available childhood ALL cell lines representing diverse immunotypes and genetic profiles. Using these cell lines, we performed comprehensive multi-omic analyses, providing proteomic, transcriptomic and pharmacoproteomic characterization of childhood ALL. We used this resource to characterize the functional impact of genetic fusions and cellular differentiation states on the proteome. Additionally, we identified a novel drug vulnerability in one of the ALL subtypes. Our results are provided as an interactive online data portal with navigable proteomics, transcriptomics, and drug sensitivity profiles.

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Citric acid, an ovarian cancer metabolite, induces pyroptosis via caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer

Project description:Malignant tumors display profound changes in cellular metabolism, yet how these altered metabolites affect the development and growth of tumors is not fully understood. Here, we used metabolomics to analyze the metabolic profile differences in ovarian cancer, and found that citric acid (CA) is the most significantly downregulated metabolite. Recently, CA has been reported to inhibit the growth of a variety of tumor cells, but whether it is involved in pyroptosis of ovarian cancer and its potential molecular mechanisms still remains to be further investigated. Here, we demonstrated that CA inhibits the growth of ovarian cancer cells in a dose-dependent manner. RNA-seq analysis revealed that CA significantly promoted the expression of thioredoxin interacting protein (TXNIP) and caspase-4 (CASP4). Morphologic examination by transmission electron microscopy indicated that CA-treated ovarian cancer cells exhibited typical pyroptosis characteristics. Further mechanistic analyses showed that CA facilitates pyroptosis via CASP4/TXNIP-NLRP3-Gesdermin-d (GSDMD) pathway in ovarian cancer. This study elucidated that CA induces ovarian cancer cell death through classical and non-classical pyroptosis pathways, which may be beneficial as an ovarian cancer therapy.

2022-08-01 | GSE189851 | GEO

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Project description:In cancer patients, metastasis of tumors to sentinel lymph nodes (LN) predicts disease progression and often guides treatment decisions. The mechanisms underlying tumor LN metastasis are poorly understood. Using comparative transcriptomics and metabolomics analyses of primary and LN metastatic tumors in mice, we found that LN metastasis requires that tumor cells undergo a metabolic shift toward fatty acid oxidation (FAO). Transcriptional co-activator yes-associated protein (YAP) is selectively activated in LN metastatic tumors, leading to upregulation of genes in the FAO signaling pathway. Pharmacological inhibition of FAO or genetic ablation of YAP suppressed LN metastasis in mice. Several bioactive bile acids were highly accumulated in the LN metastatic tumor. Inhibition of FAO or YAP may merit exploration as therapeutic strategies for mitigating tumor LN metastasis.

2019-02-09 | E-MTAB-7621 | biostudies-arrayexpress

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