Evidence map›Paper›PMID 41527462›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

GOT1 Inhibition Induces Extracellular Matrix Remodeling in Pancreatic Cancer.

Rodrigo Curvello, Sandra Hauser, Michael Seifert, Christopher K Barlow, Joel R Steele, Emma Salisbury, Daniel Croagh, Kathryn S Stok, Anna V Taubenberger, Ralf B Schittenhelm and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

11 authors.

Rodrigo CurvelloDepartment of Chemical and Biological Engineering, Faculty of Engineering, Monash University, Clayton, Australia.ORCID https://orcid.org/0000-0002-0520-4075
Sandra HauserInstitute of Radiopharmaceutical Cancer Research, Helmholtz-Zentrum Dresden-Rossendorf, Department of Radiopharmaceutical and Chemical Biology, Dresden, Germany.
Michael SeifertInstitute for Medical Informatics and Biometry (IMB), Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Christopher K BarlowMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Joel R SteeleMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Emma SalisburyDepartment of Chemical and Biological Engineering, Faculty of Engineering, Monash University, Clayton, Australia.
Daniel CroaghDepartment of Upper GI and Hepatobiliary Surgery, Monash Medical Centre, Clayton, Australia.
Kathryn S StokDepartment of Biomedical Engineering, The University of Melbourne, Parkville, Australia.
Anna V TaubenbergerBiotechnology Center, Center for Molecular and Cellular Bioengineering, Technische Universität Dresden, Dresden, Germany.
Ralf B SchittenhelmMonash Proteomics and Metabolomics Platform, Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia.
Daniela LoessnerDepartment of Chemical and Biological Engineering, Faculty of Engineering, Monash University, Clayton, Australia.ORCID https://orcid.org/0000-0001-5891-3441

Funding

HORIZON EUROPE Reforming and enhancing the European Research and Innovation system 864253National Health and Medical Research Council 2020911
6 · The paper itself

Abstract

Pancreatic cancer cells rely on glutamine to sustain their survival in the stiff and poorly vascularized tumor microenvironment (TME). Inhibiting glutamic-oxaloacetic transaminase 1 (GOT1) is a strategy to target glutamine metabolism and impair cancer cell functions. However, it remains unclear how cellular and extracellular elements of the TME respond to GOT1 inhibition. We engineered a pancreatic TME model 'on a dish' and recreated the metabolic interactions. Stromal cells remodeled the extracellular matrix and upregulated metabolic programs, including glutamine metabolism, oxidative phosphorylation, and central carbon metabolism. Cell responses to GOT1 inhibition were modulated by TME elements, with reductions in cell viability and proliferation occurring only under tissue-like conditions. GOT1 inhibition altered matrix organization by upregulating different matrix-related proteins, while it did not enhance cell responses to cytotoxic drugs. Our findings uncover the metabolic crosstalk within the TME and show that metabolism-targeting treatments directly impact stromal elements of pancreatic cancer.

Indexed as

Aspartate Aminotransferase, CytoplasmicExtracellular MatrixPancreatic NeoplasmsTumor MicroenvironmentCell Line, TumorCell ProliferationGlutamineHumansMetabolic ReprogrammingStromal CellsAspartate Aminotransferase, CytoplasmicGlutamineGOT1 protein, humanextracellular matrixmetabolismpancreatic cancerstromal cellstissue engineering

Identifiers

PMID41527462
PMCPMC12955881

What Socratic 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 Socratic graph.