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Updated: Jul 16, 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, NY 11794, USA.

Biorxiv : the Preprint Server for Biology
|September 21, 2023
PubMed

Insights

Oncogenic KRAS mutations are common in cancer. This study identifies STAT3 as a key player in regulating cancer cell traits, impacting tumor maintenance and potentially guiding new therapies for KRAS-mutant cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Oncogenic KRAS mutations are prevalent in various cancers, often linked to aggressive phenotypes and treatment resistance.
  • The epithelial-to-mesenchymal transition (EMT) is associated with cancer progression, but its mechanistic link to mutant KRAS is not fully understood.

Approach:

  • Investigated the role of STAT3 in TGF-beta-induced EMT in pancreatic cancer cells.
  • Utilized gene expression profiling to identify genes co-regulated by STAT3 and oncogenic KRAS.
  • Analyzed the functional implications of STAT3-activated gene programs in tumor maintenance and epithelial homeostasis.

Key Points:

  • STAT3 acts as a genetic modifier of TGF-beta-induced EMT.
  • Over 200 genes are commonly regulated by STAT3 and oncogenic KRAS in pancreatic cancer.
  • STAT3-regulated gene signatures reflect characteristics of human KRAS-mutant tumors.

Conclusions:

  • STAT3 plays a significant role in tumor maintenance and epithelial homeostasis in the context of KRAS mutations.
  • STAT3-mediated pathways are relevant to understanding KRAS-driven cancer aggressiveness.
  • These findings suggest potential therapeutic strategies targeting STAT3 in KRAS-mutant cancers.
Keywords:
KRAScancer dependencyepithelial carcinogenesis

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