Evidence map›Paper›PMID 30122555›Full record

ArticleCell metabolism2018

Cytosolic Aspartate Availability Determines Cell Survival When Glutamine Is Limiting.

H Furkan Alkan, Katharina E Walter, Alba Luengo, Corina T Madreiter-Sokolowski, Sarah Stryeck, Allison N Lau, Wael Al-Zoughbi, Caroline A Lewis, Craig J Thomas, Gerald Hoefler and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

126 citing papers in PubMed, 227 citations in OpenAlex.

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66 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 2 countries.

H Furkan AlkanInstitute of Biochemistry, Graz University of Technology, Humboldtstrasse 46/III, 8010 Graz, Austria; The Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Katharina E WalterInstitute of Biochemistry, Graz University of Technology, Humboldtstrasse 46/III, 8010 Graz, Austria.
Alba LuengoThe Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Corina T Madreiter-SokolowskiGottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstrasse 6/6, A-8010 Graz, Austria.
Sarah StryeckGottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstrasse 6/6, A-8010 Graz, Austria.
Allison N LauThe Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Wael Al-ZoughbiDiagnostic and Research Institute of Pathology, Medical University of Graz, Neue Stiftingtalstraße 6, A-8010 Graz, Austria.
Caroline A LewisWhitehead Institute for Biomedical Research, 455 Main Street, Cambridge, MA 02142, USA.
Craig J ThomasDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892, USA; Lymphoid Malignancies Branch, National Cancer Institute, Bethesda, MD 20892, USA.
Gerald HoeflerDiagnostic and Research Institute of Pathology, Medical University of Graz, Neue Stiftingtalstraße 6, A-8010 Graz, Austria; BioTechMed-Graz, Graz, Austria.
Wolfgang F GraierGottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstrasse 6/6, A-8010 Graz, Austria; BioTechMed-Graz, Graz, Austria.
Tobias MadlGottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstrasse 6/6, A-8010 Graz, Austria; BioTechMed-Graz, Graz, Austria.
Matthew G Vander HeidenThe Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Dana-Farber Cancer Institute, Boston, MA 02115, USA. Electronic address: mvh@mit.edu.
Juliane G Bogner-StraussInstitute of Biochemistry, Graz University of Technology, Humboldtstrasse 46/III, 8010 Graz, Austria; BioTechMed-Graz, Graz, Austria. Electronic address: juliane.bogner-strauss@tugraz.at.
Medical University of Graz · ATGraz University of Technology · ATMassachusetts Institute of Technology · USDana-Farber Cancer Institute · USNational Institutes of Health · USWhitehead Institute for Biomedical Research · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Analysis of cancer cell metabolism in diverse environmental conditionsR01CA201276 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VANDER HEIDEN, MATTHEW G., VITKUP, DENNIS · 2016 to 2020
$3.0M
Regulation of glucose metabolism to allow tumor initiation and growthR01CA168653 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2013 to 2019
$1.9M
Understanding metabolic heterogeneity in pancreatic cancerK99CA234221 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAU, ALLISON N · 2018 to 2020
$386k
Austrian Science Fund FWF F 3018Austrian Science Fund FWF J 4205Austrian Science Fund FWF P 27108Austrian Science Fund FWF P 28854Austrian Science Fund FWF W 1226Howard Hughes Medical InstituteNCI NIH HHS K99 CA234221NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA168653NCI NIH HHS R01 CA201276NIGMS NIH HHS T32 GM007287
6 · The paper itself

Abstract

Mitochondrial function is important for aspartate biosynthesis in proliferating cells. Here, we show that mitochondrial aspartate export via the aspartate-glutamate carrier 1 (AGC1) supports cell proliferation and cellular redox homeostasis. Insufficient cytosolic aspartate delivery leads to cell death when TCA cycle carbon is reduced following glutamine withdrawal and/or glutaminase inhibition. Moreover, loss of AGC1 reduces allograft tumor growth that is further compromised by treatment with the glutaminase inhibitor CB-839. Together, these findings argue that mitochondrial aspartate export sustains cell survival in low-glutamine environments and AGC1 inhibition can synergize with glutaminase inhibition to limit tumor growth.

Indexed as

Cell SurvivalAmino Acid Transport Systems, AcidicAnimalsAntiportersAspartic AcidCell LineCell ProliferationCitric Acid CycleCytosolFemaleGlutamineHumansMice, Inbred C57BLMitochondriaNeoplasmsAmino Acid Transport Systems, AcidicAntiportersaspartate-glutamate carrierAspartic AcidGlutamineAGC1Aralaraspartate-glutamate carriercancer metabolismglutamine metabolismSLC25A12

Identifiers

PMID30122555
PMCPMC6390946
OpenAlexW2885885985

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.