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GOT1 Inhibition Induces Extracellular Matrix Remodeling in Pancreatic Cancer.

Rodrigo Curvello1, Sandra Hauser2, Michael Seifert3

  • 1Department of Chemical and Biological Engineering, Faculty of Engineering, Monash University, Clayton, Australia.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 13, 2026
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Summary
This summary is machine-generated.

Inhibiting glutamic-oxaloacetic transaminase 1 (GOT1) impacts pancreatic cancer cell survival by altering tumor microenvironment (TME) metabolism and matrix organization. This highlights TME

Keywords:
extracellular matrixmetabolismpancreatic cancerstromal cellstissue engineering

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Area of Science:

  • Oncology
  • Cancer Metabolism
  • Tumor Microenvironment (TME) Research

Background:

  • Pancreatic cancer cells depend on glutamine for survival within the challenging tumor microenvironment (TME).
  • Targeting glutamine metabolism via glutamic-oxaloacetic transaminase 1 (GOT1) inhibition is a potential therapeutic strategy.
  • The impact of GOT1 inhibition on cellular and extracellular TME components remains largely unexplored.

Purpose of the Study:

  • To investigate the effects of GOT1 inhibition on the pancreatic TME.
  • To elucidate the metabolic crosstalk between cancer cells and stromal cells within the TME.
  • To understand how TME elements modulate cancer cell responses to GOT1 inhibition.

Main Methods:

  • Engineered a pancreatic TME model 'on a dish' to simulate tissue-like conditions and metabolic interactions.
  • Analyzed cellular and extracellular matrix remodeling in response to GOT1 inhibition.
  • Assessed changes in metabolic programs, cell viability, proliferation, and matrix organization.

Main Results:

  • Stromal cells within the TME remodeled the extracellular matrix and upregulated key metabolic pathways.
  • GOT1 inhibition reduced pancreatic cancer cell viability and proliferation specifically under tissue-like conditions.
  • GOT1 inhibition altered matrix organization by upregulating matrix-related proteins but did not improve responses to cytotoxic drugs.

Conclusions:

  • Metabolic crosstalk within the TME significantly influences cancer cell responses to GOT1 inhibition.
  • GOT1 inhibition directly impacts stromal components of the pancreatic TME, affecting matrix organization.
  • Targeting cancer metabolism offers a novel approach to modulate the TME in pancreatic cancer.