Summary of Study ST002578

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001663. The data can be accessed directly via it's Project DOI: 10.21228/M8R72W This work is supported by NIH grant, U2C- DK119886.


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 IDST002578
Study TitleSteady State Metabolomics Study in SMARCA4 mutant(BIN-67) cells cultured in the absence of glucose or glutamine
Study Summarysteady-state abundances of all TCA cycle intermediates were more severely reduced in BIN-67 cells deprived of glutamine than those deprived of glucose
McGill University
LaboratorySidong Huang Lab
Last NameFu
First NameZheng
AddressMcIntyre Medical Sciences Building, 3655 promenade Sir-William-Osler
Submit Date2023-04-24
Raw Data AvailableYes
Raw Data File Type(s)mzXML
Analysis Type DetailGC-MS
Release Date2023-05-22
Release Version1
Zheng Fu Zheng Fu application/zip

Select appropriate tab below to view additional metadata details:


Project ID:PR001663
Project DOI:doi: 10.21228/M8R72W
Project Title:Alanine supplementation exploits glutamine dependency induced by SMARCA4/2-loss
Project Summary:SMARCA4 (BRG1) and SMARCA2 (BRM) are the two paralogous ATPases of the SWI/SNF chromatin remodeling complexes frequently inactivated in cancers.we uncover that SMARCA4/2-loss represses expression of the glucose transporter GLUT1, causing reduced glucose uptake and glycolysis accompanied with increased dependency on oxidative phosphorylation (OXPHOS); adapting to this, these SMARCA4/2-deficient cells rely on elevated SLC38A2, an amino acid transporter, to increase glutamine import for fueling OXPHOS. Consequently, SMARCA4/2-deficient cells and tumors are highly sensitive to inhibitors targeting OXPHOS or glutamine metabolism. Furthermore, supplementation of alanine, also imported by SLC38A2, restricts glutamine uptake through competition and selectively induces death in SMARCA4/2-deficient cancer cells. At a clinically relevant dose, alanine supplementation synergizes with OXPHOS inhibition or conventional chemotherapy eliciting marked antitumor activity in patient-derived xenografts. Our findings reveal multiple druggable vulnerabilities of SMARCA4/2-loss exploiting a GLUT1/SLC38A2-mediated metabolic shift. Particularly, unlike dietary deprivation approaches, alanine supplementation can be readily applied to current regimens for better treatment of these aggressive cancers.
Institute:McGill University
Laboratory:Sidong Huang Lab
Last Name:Fu
First Name:Zheng
Address:McIntyre Medical Sciences Building