Evidence map›Paper›PMID 30122553›Full record

ArticleCell metabolism2018

A Role for p53 in the Adaptation to Glutamine Starvation through the Expression of SLC1A3.

Mylène Tajan, Andreas K Hock, Julianna Blagih, Neil A Robertson, Christiaan F Labuschagne, Flore Kruiswijk, Timothy J Humpton, Peter D Adams, Karen H Vousden

Open access · hybridAbstract 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 152 papers.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

152 citing papers in PubMed, 220 citations in OpenAlex.

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  8. The hidden players: LncRNA-Encoded micropeptides in cancer hallmarks.Cellular and molecular life sciences : CMLS · 2026
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92 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

9 authors at 4 institutions in 2 countries.

Mylène TajanThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Andreas K HockCancer Research UK Beatson Institute, Switchback Road, Glasgow G61 1BD, UK.
Julianna BlagihThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Neil A RobertsonInstitute of Cancer Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1BD, UK.
Christiaan F LabuschagneThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Flore KruiswijkCancer Research UK Beatson Institute, Switchback Road, Glasgow G61 1BD, UK.
Timothy J HumptonCancer Research UK Beatson Institute, Switchback Road, Glasgow G61 1BD, UK.
Peter D AdamsInstitute of Cancer Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1BD, UK; Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Karen H VousdenThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK. Electronic address: karen.vousden@crick.ac.uk.
The Francis Crick Institute · GBCancer Research UK · GBSanford Burnham Prebys Medical Discovery Institute · USUniversity of Glasgow · GB

Funding

Cancer Research UK 16566Cancer Research UK 18274Cancer Research UK C10652/A16566Cancer Research UK C596/A10419Cancer Research UK C596/A26855Medical Research CouncilWellcome Trust
6 · The paper itself

Abstract

Numerous mechanisms to support cells under conditions of transient nutrient starvation have been described. Several functions of the tumor-suppressor protein p53 can contribute to the adaptation of cells to metabolic stress and help cancer cell survival under nutrient-limiting conditions. We show here that p53 promotes the expression of SLC1A3, an aspartate/glutamate transporter that allows the utilization of aspartate to support cells in the absence of extracellular glutamine. Under glutamine deprivation, SLC1A3 expression maintains electron transport chain and tricarboxylic acid cycle activity, promoting de novo glutamate, glutamine, and nucleotide synthesis to rescue cell viability. Tumor cells with high levels of SLC1A3 expression are resistant to glutamine starvation, and SLC1A3 depletion retards the growth of these cells in vitro and in vivo, suggesting a therapeutic potential for SLC1A3 inhibition.

Indexed as

Adaptation, PhysiologicalAnimalsCell Line, TumorCell SurvivalCitric Acid CycleExcitatory Amino Acid Transporter 1FemaleGlutamineHumansMice, Inbred BALB CNeoplasmsStarvationTumor Suppressor Protein p53Excitatory Amino Acid Transporter 1GlutamineSLC1A3 protein, humanSlc1a3 protein, mouseTumor Suppressor Protein p53aspartate metabolismglutamine starvationp53SLC1A3

Identifiers

PMID30122553
PMCPMC6224545
OpenAlexW2885597648

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.