Summary of Study ST002856

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.

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Study IDST002856
Study TitleValidation of on-target effect of IACS-010759 in vehicle- and Enzalutamide-treated 16D cells
Study SummaryIn this study, we sought to validate that 30nM IACS-010759, a complex I inhibitor, had an on-target effect in vehicle- and Enzalutamide-treated 16D prostate cancer cells.
Institute
University of California, Los Angeles
LaboratoryGoldstein Lab
Last NameGiafaglione
First NameJenna
Address610 Charles E Young Dr S, Los Angeles, CA, 90024, USA
Emailjgiafaglione@g.ucla.edu
Phone408-728-3065
Submit Date2023-09-11
Raw Data AvailableYes
Raw Data File Type(s)d
Analysis Type DetailGC-MS
Release Date2023-09-13
Release Version1
Jenna Giafaglione Jenna Giafaglione
https://dx.doi.org/10.21228/M8KX5C
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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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
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