Evidence map›Paper›PMID 39843491›Full record

ArticleScientific reports2025

SLC1A5 is a key regulator of glutamine metabolism and a prognostic marker for aggressive luminal breast cancer.

Lutfi H Alfarsi, Rokaya El Ansari, Busra Erkan, Ali Fakroun, Madeleine L Craze, Mohammed A Aleskandarany, Kiu Wai Cheng, Ian O Ellis, Emad A Rakha, Andrew R Green

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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  12. Targeting glutamine metabolism as a potential target for cancer treatment.Journal of experimental & clinical cancer research : CR · 2025
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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

10 authors.

Lutfi H AlfarsiNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Rokaya El AnsariNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Busra ErkanNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Ali FakrounNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Madeleine L CrazeNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Mohammed A AleskandaranyNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Kiu Wai ChengNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Ian O EllisNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Emad A RakhaNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England.
Andrew R GreenNottingham Breast Cancer Research Centre, Academic Unit of Translational Medical Sciences, School of Medicine, University of Nottingham, University of Nottingham Biodiscovery Institute, University Park, Nottingham, NG7 2RD, England. andrew.green@nottingham.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells exhibit altered metabolism, often relying on glutamine (Gln) for growth. Breast cancer (BC) is a heterogeneous disease with varying clinical outcomes. We investigated the role of the amino acid transporter SLC1A5 (ASCT2) and its association with BC subtypes and patient outcomes. In large BC cohorts, SLC1A5 mRNA (n = 9488) and SLC1A5 protein (n = 1274) levels were assessed and correlated their expression with clinicopathological features, molecular subtypes, and patient outcomes. In vitro SLC1A5 knockdown and inhibition studies in luminal BC cell lines (ZR-75-1 and HCC1500) were used to further explore the role of SLC1A5 in Gln metabolism. Statistical analysis was performed using chi-squared tests, ANOVA, Spearman's correlation, Kaplan-Meier analysis, and Cox regression. SLC1A5 mRNA and SLC1A5 protein expression were strongly correlated in luminal B, HER2 + and triple-negative BC (TNBC). Both high SLC1A5 mRNA and SLC1A5 protein expression were associated with larger tumour size, higher grade, and positive axillary lymph node metastases (P < 0.01). Importantly, high SLC1A5 expression correlated with poor BC-specific survival specifically in the highly proliferative luminal subtype (P < 0.001). Furthermore, SLC1A5 knockdown by siRNA or GPNA inhibition significantly reduced cell proliferation and glutamine uptake in ZR-75-1 cells. Our findings suggest SLC1A5 plays a key role in the aggressive luminal BC subtype and represents a potential therapeutic target. Further research is needed to explore SLC1A5 function in luminal BC and its association with Gln metabolism pathways.

Indexed as

Amino Acid Transport System ASCBiomarkers, TumorBreast NeoplasmsGlutamineMinor Histocompatibility AntigensAdultAgedCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMiddle AgedPrognosisAmino Acid Transport System ASCBiomarkers, TumorGlutamineMinor Histocompatibility AntigensSLC1A5 protein, humanBreast cancerPrognosisSLC1A5Tumour marker

Identifiers

PMID39843491
PMCPMC11754656

What OpenQuestion holds

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Registered trials

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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.