Summary of Study ST002865

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.

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Study IDST002865
Study TitleMetabolic profiling, glucose tracing and glutamine tracing in 16D prostate cancer cells treated with vehicle, AR inhibitor Enzalutamide, AR inhibitor Apalutamide, or AR degrader/PROTAC ARCC-4
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 Date2023-09-12
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

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Factors:

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

mb_sample_id local_sample_id Treatment
SA309483NN.009Apalutamide_C13Glc
SA309484NN.008Apalutamide_C13Glc
SA309485NN.007Apalutamide_C13Glc
SA309486NN.019Apalutamide_C13Gln
SA309487NN.021Apalutamide_C13Gln
SA309488NN.020Apalutamide_C13Gln
SA309477NN.012ARCC4_C13Glc
SA309478NN.010ARCC4_C13Glc
SA309479NN.011ARCC4_C13Glc
SA309480NN.022ARCC4_C13Gln
SA309481NN.024ARCC4_C13Gln
SA309482NN.023ARCC4_C13Gln
SA309489NN.005Enzalutamide_C13Glc
SA309490NN.004Enzalutamide_C13Glc
SA309491NN.006Enzalutamide_C13Glc
SA309492NN.018Enzalutamide_C13Gln
SA309493NN.017Enzalutamide_C13Gln
SA309494NN.016Enzalutamide_C13Gln
SA309495QC.blank1NA
SA309496QC.blank2NA
SA309497QC.blank3NA
SA309498NN.003Vehicle_C13Glc
SA309499NN.001Vehicle_C13Glc
SA309500NN.002Vehicle_C13Glc
SA309501NN.014Vehicle_C13Gln
SA309502NN.013Vehicle_C13Gln
SA309503NN.015Vehicle_C13Gln
Showing results 1 to 27 of 27
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