Summary of Study ST002115
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 PR001340. The data can be accessed directly via it's Project DOI: 10.21228/M8HD8Q This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST002115 |
| Study Title | LC-MS analysis of metabolic changes induced by GPX4 inhibitor treatment in cultured HT1080 cells |
| Study Summary | HT1080 cells were treated with vehicle (DMSO), RSL3 (10 micromolar), ML210 (10 micromolar), or ML162 (10 micromolar) for 2 hours. Cellular metabolites were then extracted and analyzed by LC-MS. |
| Institute | University of Texas MD Anderson Cancer Center |
| Last Name | Gan |
| First Name | Boyi |
| Address | 6565 MD Anderson Blvd, Houston TX, 77030 |
| bgan@mdanderson.org | |
| Phone | 713-792-8653 |
| Submit Date | 2022-03-02 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | mzXML |
| Analysis Type Detail | LC-MS |
| Release Date | 2022-04-14 |
| Release Version | 1 |
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Project:
| Project ID: | PR001340 |
| Project DOI: | doi: 10.21228/M8HD8Q |
| Project Title: | A ferroptosis defense mechanism mediated by glycerol 3-phosphate dehydrogenase 2 in mitochondria |
| Project Summary: | Mechanisms of defense against ferroptosis (an iron-dependent form of cell death induced by lipid peroxidation) in cellular organelles remain poorly understood, hindering our ability to target ferroptosis in disease treatment. In this study, metabolomic analyses revealed that treatment of cancer cells with glutathione peroxidase 4 (GPX4) inhibitors results in intracellular glycerol 3-phosphate (G3P) depletion. We further showed that supplementation of cancer cells with G3P attenuates ferroptosis induced by GPX4 inhibitors in a G3P dehydrogenase 2 (GPD2)-dependent manner; GPD2 deletion sensitizes cancer cells to GPX4 inhibition-induced mitochondrial lipid peroxidation and ferroptosis, and combined deletion of GPX4 and GPD2 synergistically suppresses tumor growth by inducing ferroptosis in vivo. Mechanistically, inner mitochondrial membrane-localized GPD2 couples G3P oxidation with ubiquinone reduction to ubiquinol, which acts as a radical-trapping antioxidant to suppress ferroptosis in mitochondria. Taken together, these results reveal that GPD2 participates in ferroptosis defense in mitochondria by generating ubiquinol. |
| Institute: | University of Texas MD Anderson Cancer Center |
| Last Name: | Gan |
| First Name: | Boyi |
| Address: | 6565 MD Anderson Blvd, Houston, TX 77030 |
| Email: | bgan@mdanderson.org |
| Phone: | 713-792-8653 |
