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Updated: Jun 29, 2025

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STAT3 is a genetic modifier of TGF-beta induced EMT in KRAS mutant pancreatic cancer

Stephen D'Amico1, Varvara Kirillov1, Oleksi Petrenko1

  • 1Department of Microbiology and Immunology, Stony Brook University, Stony Brook, United States.

Elife
|April 4, 2024
PubMed

Insights

STAT3 modifies epithelial to mesenchymal transition in KRAS-mutant cancers. This STAT3-driven program is crucial for tumor maintenance and reflects human pancreatic cancer characteristics, impacting aggressiveness and therapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Oncogenic KRAS mutations are prevalent in many cancers, often correlating with increased aggressiveness and therapy resistance.
  • The epithelial-to-mesenchymal transition (EMT) is linked to cancer progression, but its mechanistic connection to mutant KRAS is not fully understood.

Purpose of the Study:

  • To elucidate the mechanistic link between mutant KRAS and cancer aggressiveness phenotypes.
  • To identify genetic modifiers of TGF-beta-induced EMT in the context of KRAS mutations.

Main Methods:

  • Gene expression profiling of pancreatic cancer cells.
  • Analysis of STAT3 and KRAS co-regulated genes.
  • Functional classification of gene signatures.

Main Results:

  • STAT3 was identified as a genetic modifier of TGF-beta-induced EMT.
  • Over 200 genes were found to be commonly regulated by STAT3 and oncogenic KRAS.
  • The STAT3-responsive gene program is critical for tumor maintenance and epithelial homeostasis.

Conclusions:

  • STAT3 plays a significant role in KRAS-driven cancer progression and EMT.
  • The identified STAT3-activated gene signatures are relevant to human KRAS-mutant tumors.
  • These findings have implications for understanding tumor aggressiveness and developing novel therapeutic strategies.
Keywords:
KRASSTAT3cancer biologycancer dependencyepithelial carcinogenesismouse

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