Summary of Study ST000465

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000357. The data can be accessed directly via it's Project DOI: 10.21228/M8WW32 This work is supported by NIH grant, U2C- DK119886.

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Study IDST000465
Study TitleUniquely Tumor-Selective Englerin A Profoundly Alters Lipid Metabolism in Renal Cell Carcinoma inducing ER-Stress and an Acute Inflammatory Response
Study TypeMetabolomic effect of Englerin A on renal cell carcinoma
Study SummaryThis targeted metabolomic analysis was performed on renal cell carcinoma A498 cells with or without anti-cancer drug Englerin treatment for 24 and 48 h.
Institute
University of California, San Diego
DepartmentDepartment of Pediatrics
Last NameBatova
First NameAyse
AddressLa Jolla, CA 92093
Emailabatova@ucsd.edu
Phone619-543-1962
Submit Date2016-09-09
Num GroupsTwo groups for 24 h treatment (control and Eglerin treatment) and two groups for 48 h treatment. Each has 4 replicates
Total Subjects16
Analysis Type DetailLC-MS
Release Date2016-12-22
Release Version1
Ayse Batova Ayse Batova
https://dx.doi.org/10.21228/M8WW32
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000357
Project DOI:doi: 10.21228/M8WW32
Project Title:Uniquely Tumor-Selective Englerin A Profoundly Alters Lipid Metabolism in Renal Cell Carcinoma inducing ER-Stress and an Acute Inflammatory Response
Project Type:Cancer cell
Project Summary:Renal cell carcinoma (RCC) is among the top ten most common forms of cancer and is the most common malignancy of the kidney. Screening of plant extracts in search of new anti-cancer agents resulted in the discovery of englerin A, a guaiane sesquiterpene with potent cytotoxicity against renal cancer cells and a small subset of other cancer cells. the current study used a systems biology approach to explore the mechanism(s) of action of engerin A at a more global level.Our metabolomics analyses indicated that englerin A profoundly altered lipid metabolism in cc-RCC cell lines and generated significant levels of ceramides that were highly toxic to these cells. Microarray analyses determined that englerin A induced ER stress signaling and an acute inflammatory response, which was confirmed by quantitative PCR and Western Blot analyses.Our findings suggest that cc-RCC is highly sensitive to disruptions in lipid metabolism and ER stress and that these vulnerabilities can be targeted for the treatment of cc-RCC and possibly other lipid storing cancers.
Institute:University of California, San Diego
Department:Department of Pediatrics
Last Name:Batova
First Name:Ayse
Address:La Jolla, CA 92093
Email:abatova@ucsd.edu
Phone:619-543-1962
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