Summary of Study ST002860
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 PR001788. The data can be accessed directly via it's Project DOI: 10.21228/M8KX5C 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 | ST002860 |
| Study Title | Glucose tracing in vehicle- and Enzalutamide-treated 16D prostate cancer cells (replicates 2 and 3) |
| Study Summary | In this study, we sought to determine how Enzalutamide treatment alters metabolism in 16D prostate cancer cells (replicates 2 and 3). |
| Institute | University of California, Los Angeles |
| Laboratory | Goldstein Lab |
| Last Name | Giafaglione |
| First Name | Jenna |
| Address | 610 Charles E Young Dr S, Los Angeles, CA, 90024, USA |
| jgiafaglione@g.ucla.edu | |
| Phone | 408-728-3065 |
| Submit Date | 2023-09-12 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | d |
| Analysis Type Detail | GC-MS |
| Release Date | 2023-09-15 |
| Release Version | 1 |
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Project:
| Project ID: | PR001788 |
| Project DOI: | doi: 10.21228/M8KX5C |
| Project Title: | MYC is a regulator of AR inhibition-induced metabolic requirements in prostate cancer |
| Project Summary: | Advanced prostate cancers are treated with therapies targeting the androgen receptor (AR) signaling pathway. While many tumors initially respond to AR inhibition, nearly all develop resistance. It is critical to understand how prostate tumor cells respond to AR inhibition in order to exploit therapy-induced phenotypes prior to the outgrowth of treatment-resistant disease. Here, we comprehensively characterize the effect of AR blockade on prostate cancer metabolism using transcriptomics, metabolomics and bioenergetics approaches. The metabolic response to AR inhibition is defined by reduced glycolysis, robust elongation of mitochondria, and increased reliance on mitochondrial oxidative metabolism. We establish DRP1 activity and MYC signaling as mediators of AR blockade-induced metabolic phenotypes. Rescuing DRP1 phosphorylation after AR inhibition restores mitochondrial fission, while rescuing MYC restores glycolytic activity and prevents sensitivity to complex I inhibition. Our study provides new insight into the regulation of treatment-induced metabolic phenotypes and vulnerabilities in prostate cancer. |
| Institute: | UCLA |
| Laboratory: | Goldstein Lab |
| Last Name: | Giafaglione |
| First Name: | Jenna |
| Address: | 610 Charles E Young Dr S, Los Angeles, CA, 90024, USA |
| Email: | jgiafaglione@g.ucla.edu |
| Phone: | 408-728-3065 |
