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

Select appropriate tab below to view additional metadata details:


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

Subject:

Subject ID:SU002968
Subject Type:Cultured cells
Subject Species:Homo sapiens
Taxonomy ID:9606

Factors:

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

mb_sample_id local_sample_id Treatment
SA308790LT Enza-IACS-230nM IACS-010759
SA308791LT Enza-IACS-130nM IACS-010759
SA308792Naive-IACS-330nM IACS-010759
SA308793Naive-IACS-130nM IACS-010759
SA308794Naive-IACS-230nM IACS-010759
SA308795LT Enza-IACS-330nM IACS-010759
SA308796LT Enza-NT3Vehicle (DMSO)
SA308797LT Enza-NT1Vehicle (DMSO)
SA308798Naive-NT2Vehicle (DMSO)
SA308799Naive-NT3Vehicle (DMSO)
SA308800Naive-NT1Vehicle (DMSO)
SA308801LT Enza-NT2Vehicle (DMSO)
Showing results 1 to 12 of 12

Collection:

Collection ID:CO002961
Collection Summary:Vehicle- and Enzalutamide-treated 16D cells were cultured with 30nM IACS-010759 for 24 hours
Sample Type:Cultured cells

Treatment:

Treatment ID:TR002977
Treatment Summary:Vehicle- and Enzalutamide-treated 16D cells were cultured with 30nM IACS-010759 in U13C-glucose-containing media for 24 hours

Sample Preparation:

Sampleprep ID:SP002974
Sampleprep Summary:Cell plates were placed on ice and quickly washed with ice-cold 0.9% (w/v) NaCl. Cells were immediately treated with 500 μL of ice-cold MeOH and 200 μL water containing 1 μg of the internal standard norvaline. Cells were then scraped and placed in 1.5 mL centrifuge tubes kept on ice. Next, 500 μL of chloroform was added, after which samples were vortexed for 1 minute and then spun at 10,000g for 5 minutes at 4C. The aqueous layer was transferred to a GC/MS sample vial and dried overnight using a refrigerated CentriVap.

Combined analysis:

Analysis ID AN004678
Analysis type MS
Chromatography type GC
Chromatography system Agilent 7890A
Column Agilent DB5-MS (30m x 0.25mm, 0.25um)
MS Type EI
MS instrument type Single quadrupole
MS instrument name Agilent 5977B
Ion Mode POSITIVE
Units abundance

Chromatography:

Chromatography ID:CH003520
Instrument Name:Agilent 7890A
Column Name:Agilent DB5-MS (30m x 0.25mm, 0.25um)
Column Temperature:23
Flow Gradient:N/A (GC-MS)
Flow Rate:1 ml/min
Solvent A:N/A (GC-MS)
Solvent B:N/A (GC-MS)
Chromatography Type:GC

MS:

MS ID:MS004425
Analysis ID:AN004678
Instrument Name:Agilent 5977B
Instrument Type:Single quadrupole
MS Type:EI
MS Comments:Data was analyzed using Agilent MassHunter software. Stable isotope tracing data was corrected for natural abundance of heavy isotopes with FluxFix software using a reference set of unlabeled metabolite standards2.
Ion Mode:POSITIVE
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