Summary of Study ST002863

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 PR001786. The data can be accessed directly via it's Project DOI: 10.21228/M8VB1G 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.

Perform statistical analysis  |  Show all samples  |  Show named metabolites  |  Download named metabolite data  
Download mwTab file (text)   |  Download mwTab file(JSON)   |  Download data files (Contains raw data)
Study IDST002863
Study TitleMetabolic profiling and glucose tracing in naive and Enzalutamide-treated 16D prostate cancer cells
Study SummaryAdvanced 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. In the MS data, M0, M1, M2, M3,... represent isotopologues of each metabolite.
Institute
University of California, Los Angeles
DepartmentMolecular, Cell and Developmental Biology
LaboratoryAndrew Goldstein
Last NameGoldstein
First NameAndrew
Address610 Charles E Young Dr East, Goldstein Lab 3141 Terasaki Life Sci Bld, Los Angeles, CA, 90095, USA
EmailAGoldstein@mednet.ucla.edu
Phone3102061402
Submit Date2023-09-11
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2023-09-19
Release Version1
Andrew Goldstein Andrew Goldstein
https://dx.doi.org/10.21228/M8VB1G
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:


Factors:

Subject type: Cultured cells; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Treatment
SA309436JG-004Enzalutamide 24 hours
SA309437JG-006Enzalutamide 24 hours
SA309438JG-005Enzalutamide 24 hours
SA309439JG-009Enzalutamide 48 hours
SA309440JG-007Enzalutamide 48 hours
SA309441JG-008Enzalutamide 48 hours
SA309442JG-012Enzalutamide long-term
SA309443JG-010Enzalutamide long-term
SA309444JG-011Enzalutamide long-term
SA309445QC-blank2NA
SA309446QC-blank1NA
SA309447JG-002vehicle (DMSO)
SA309448JG-003vehicle (DMSO)
SA309449JG-001vehicle (DMSO)
Showing results 1 to 14 of 14
  logo