Summary of Study ST002585
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 PR001665. The data can be accessed directly via it's Project DOI: 10.21228/M8GQ6R 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 | ST002585 |
| Study Title | Zinc treatment reverses and anti-Zn-regulated miRs suppress esophageal carcinomas in vivo |
| Study Summary | Using gas chromatography time-of-flight mass spectrometry GC-TOF MS (3), we performed untargeted metabolomic profiling on esophageal mucosa of Zn-treated vs Zn-untreated rats (n = 10 rats per cohort). Thirty-eight significantly altered metabolites (24 down-, 14 up-regulated, P < 0.05) were identified in the Zn-treated vs Zn-untreated esophagus. Of the 24 down-regulated metabolites, 15 (63%) were involved in anabolic/biosynthetic pathways, including amino acid/pyrimidine/purine metabolism and polyamine biosynthesis. Putrescine (intermediate in polyamine biosynthesis), shown to be up 6.4-fold in ESCC-bearing ZD esophagus (3), was down-regulated -3.96-fold in Zn-treated esophagus. Ornithine decarboxylase (ODC) is the rate liming enzyme in the polyamine biosynthetic pathway to form putrescine, which is converted into spermidine and spermine. Polyamines are indispensable for cell proliferation/tumor growth, and depletion of polyamines inhibits tumor growth (6). Of the 14 metabolites that were significantly up-regulated in the Zn-treated esophagus, five (37%) were carbohydrates, including glucose, which is up-regulated 3.4-fold, pointing to a decreased uptake of glucose and a reversal of the Warburg effect after Zn treatment. Critical to cancer aerobic glycolysis is the metabolic enzyme hexokinase 2 (HK2) that catalyzes the first committed step in glucose metabolism where glucose is phosphorylated to form glucose-6-phosphate. HK2 overexpression accounts for the high glycolytic rate in cancer cells (7). In summary, Zn treatment that significantly reduced ESCC incidence reversed classic cancer cell metabolic phenotypes such as increased glycolysis and nucleoside intermediates, with decrease in putrescine, increase in glucose, accompanied by down-regulation of metabolite enzymes ODC and HK2. |
| Institute | West Coast Metabolomics Center |
| Last Name | Pedrosa |
| First Name | Diego |
| Address | 451 Health Science Dr, Davis, CA, 95616, USA |
| dpedrosa@ucdavis.edu | |
| Phone | (530) 752-8129 |
| Submit Date | 2023-04-20 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | cdf |
| Analysis Type Detail | GC-MS |
| Release Date | 2023-05-15 |
| Release Version | 1 |
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Collection:
| Collection ID: | CO002680 |
| Collection Summary: | At sacrifice, esophagi from Zn-treated vs Zn-untreated rats were isolated (n = 10 rats per cohort). Esophageal epithelium was prepared by using a blade to remove the submucosal and muscularis layers, snap-frozen in liquid nitrogen, and stored at –80 °C. Frozen esophageal samples from Zn-untreated and Zn-treated rats (20 mg per esophagus) were shipped on dry ice to the NIH West Coast Metabolomics Center, University of California, Davis. |
| Sample Type: | Epithelial cells |
