Evidence map›Paper›PMID 27129276›Full record

ArticleThe Journal of biological chemistry2016

Deletion of Amino Acid Transporter ASCT2 (SLC1A5) Reveals an Essential Role for Transporters SNAT1 (SLC38A1) and SNAT2 (SLC38A2) to Sustain Glutaminolysis in Cancer Cells.

Angelika Bröer, Farid Rahimi, Stefan Bröer

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
18.4field-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

166 citing papers in PubMed, 1 synthesis or guideline pooled it, 248 citations in OpenAlex.

  1. Pooled it
  2. A first-in-man PET study of 2-amino-[3-Annals of nuclear medicine · 2025
    Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. A Novel Potent and Selective GCN2 Inhibitor, APL-4098, Has Antileukemic Activity through Dysregulation of Mitochondrial Function.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Article
  19. [Glutamine metabolic reprogramming in regulating the occurrence and development of osteosarcoma].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  20. Review

106 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

3 authors at 1 institution in 1 country.

Angelika BröerFrom the Research School of Biology, The Australian National University, Canberra, Australian Capital Territory 2601, Australia.
Farid RahimiFrom the Research School of Biology, The Australian National University, Canberra, Australian Capital Territory 2601, Australia.
Stefan BröerFrom the Research School of Biology, The Australian National University, Canberra, Australian Capital Territory 2601, Australia Stefan.broeer@anu.edu.au.ORCID 0000-0002-8040-1634
Australian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many cancer cells depend on glutamine as they use the glutaminolysis pathway to generate building blocks and energy for anabolic purposes. As a result, glutamine transporters are essential for cancer growth and are potential targets for cancer chemotherapy with ASCT2 (SLC1A5) being investigated most intensively. Here we show that HeLa epithelial cervical cancer cells and 143B osteosarcoma cells express a set of glutamine transporters including SNAT1 (SLC38A1), SNAT2 (SLC38A2), SNAT4 (SLC38A4), LAT1 (SLC7A5), and ASCT2 (SLC1A5). Net glutamine uptake did not depend on ASCT2 but required expression of SNAT1 and SNAT2. Deletion of ASCT2 did not reduce cell growth but caused an amino acid starvation response and up-regulation of SNAT1 to replace ASCT2 functionally. Silencing of GCN2 in the ASCT2(-/-) background reduced cell growth, showing that a combined targeted approach would inhibit growth of glutamine-dependent cancer cells.

Indexed as

Amino Acid Transport System AAmino Acid Transport System ASCCell ProliferationGene DeletionGene ExpressionGlutamineHeLa CellsHomeostasisHumansIon TransportMetabolic Networks and PathwaysMinor Histocompatibility AntigensAmino Acid Transport System AAmino Acid Transport System ASCGlutamineMinor Histocompatibility AntigensSLC1A5 protein, humanSLC38A1 protein, humanSLC38A2 protein, humanamino acid transportcell growthglutaminemammalian target of rapamycin (mTOR)membrane transport

Identifiers

PMID27129276
PMCPMC4933233
OpenAlexW2343904188

What OpenQuestion holds

Textmetadata
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.