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Updated: Mar 19, 2026

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Stromal TGFβR2 signaling: a gateway to progression for pancreatic cancer

Moriah M Hagopian1, Rolf A Brekken1

  • 1Division of Surgical Oncology; Department of Surgery and Hamon Center for Therapeutic Oncology Research; University of Texas Southwestern Medical Center ; Dallas, TX USA.

Molecular & Cellular Oncology
|June 17, 2016
PubMed

Insights

Targeting transforming growth factor beta (TGFβ) in pancreatic cancer is complex. Inhibiting stromal TGFβ receptor 2 (Tgfβr2) effectively reduced pancreatic ductal adenocarcinoma metastasis in preclinical models.

Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Biology

Background:

  • Pancreatic ductal adenocarcinoma (PDA) progression is influenced by transforming growth factor beta (TGFβ).
  • Therapeutic targeting of the TGFβ pathway in PDA remains a significant challenge due to its complex role.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting stromal TGFβ signaling in PDA.
  • To evaluate the impact of inhibiting TGFβ receptor 2 (Tgfβr2) on epithelial plasticity and metastasis in PDA models.

Main Methods:

  • Utilized antibody-mediated inhibition of stromal Tgfβr2 in preclinical xenograft models of PDA.
  • Assessed the effects on epithelial plasticity, a key driver of cancer progression and metastasis.

Main Results:

  • Antibody-mediated inhibition of stromal Tgfβr2 prevented or reversed epithelial plasticity.
  • This inhibition led to a significant reduction in PDA metastasis in the studied xenograft models.

Conclusions:

  • Targeting stromal Tgfβr2 represents a promising therapeutic strategy for pancreatic ductal adenocarcinoma.
  • Inhibition of this pathway effectively mitigates PDA metastasis by controlling epithelial plasticity.
Keywords:
TGF-βepithelial to mesenchymal transitionmetastasispancreatic cancertumor–stroma interactions

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