Summary of Study ST001920
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 PR001211. The data can be accessed directly via it's Project DOI: 10.21228/M85Q6Z 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 | ST001920 |
| Study Title | Metabolic and lipidomic characterization of radioresistant MDA-MB-231 human breast cancer cells to investigate potential therapeutic targets |
| Study Summary | To provide preliminary insights into metabolic and lipidomic characteristics in radioresistant triple-negative breast cancer (TNBC) cells and suggest potential therapeutic targets, we performed a comprehensive metabolic and lipidomic profiling of radioresistant MDA-MB-231 (MDA-MB-231/RR) TNBC cells and their parental cells using gas chromatography-mass spectrometry and nano electrospray ionization-mass spectrometry, followed by multivariate statistical analysis. Buthionine sulfoximine (BSO) and radiation were co-treated to radioresistant TNBC cells. The level of glutathione (GSH) was significantly increased, and the levels of GSH synthesis-related metabolites, such as cysteine, glycine, and glutamine were also increased in MDA-MB-231/RR cells. In contrast, the level of lactic acid was significantly reduced. In addition, reactive oxygen species (ROS) level was decreased in MDA-MB-231/RR cells. In the lipidomic profiles of MDA-MB-231/RR cells, the levels of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were significantly increased, whereas those of most of the phosphatidylinositol species were significantly decreased. BSO sensitized MDA-MB-231/RR cells to radiotherapy, which resulted in decreased GSH level and increased ROS level and apoptosis. Radioresistant TNBC cells showed distinct metabolic and lipidomic characteristics compared to their parental cells. We suggested activated GSH, PC, and PE biosynthesis pathways as potential targets for treating radioresistant TNBC cells. Particularly, enhanced radiosensitivity was achieved by inhibition of GSH biosynthesis in MDA-MB-231/RR cells. |
| Institute | ChungAng University |
| Department | College of Pharmacy |
| Laboratory | Natural product biotechnology and Metabolomics |
| Last Name | Lee |
| First Name | Hwanhui |
| Address | College of Pharmacy, Chung-Ang University, Seoul 06974, Republic of Korea |
| hwanhui56@gmail.com | |
| Phone | +8228205605 |
| Submit Date | 2021-09-22 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo), d |
| Analysis Type Detail | GC-MS/MS(Dir. inf.) |
| Release Date | 2021-10-02 |
| Release Version | 1 |
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Treatment:
| Treatment ID: | TR002010 |
| Treatment Summary: | Cells at 70–80% confluency were subjected to irradiation using a ^60CO Theratron-780 teletherapy unit at a dose rate of 1.52 Gy per minute. The cells were subjected to 25 cycles of 2 Gy irradiation over 5 weeks, and the surviving cells were designated as MDA-MB-231/RR cells. |
| Cell Media: | DMEM supplemented with 10% FBS and 1% penicillin-streptomycin |
| Cell Envir Cond: | A humidified incubator at 37 °C (95% air and 5% CO2) |
