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Pathophysiological role of microRNA-29 in pancreatic cancer stroma

Jason J Kwon1, Sarah C Nabinger1, Zachary Vega2

  • 1Department of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA.

Scientific Reports
|June 23, 2015
PubMed

Insights

MicroRNA-29 (miR-29) loss in pancreatic cancer stroma promotes fibrotic extracellular matrix deposition. Restoring miR-29 in activated stellate cells reduces stromal buildup and pancreatic ductal adenocarcinoma progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) features a dense fibrotic stroma that hinders drug delivery and influences cancer progression.
  • Current anti-stromal therapies have not improved chemotherapy response or patient survival in PDAC.
  • Paradoxically, stroma can impede tumor progression, and its complete removal may accelerate PDAC growth.

Purpose of the Study:

  • To investigate the molecular mechanisms of tumor-stromal interactions in PDAC.
  • To determine the role of miR-29 in activated pancreatic stellate cells (PSCs) and their contribution to the fibrotic stroma.

Main Methods:

  • Utilized in vitro and in vivo models, alongside PDAC patient biopsies.
  • Conducted miR-29 gain/loss-of-function studies in PSCs.
  • Investigated the SMAD3 dependency in TGF-β1 activated PSCs.

Main Results:

  • Loss of miR-29 is a common feature in activated PSCs from PDAC.
  • Reduced miR-29 correlates with increased extracellular matrix (ECM) deposition in PDAC stroma.
  • Overexpression of miR-29 in activated stellate cells decreased stromal deposition, cancer cell viability, and tumor growth in co-culture models.
  • miR-29 loss in TGF-β1 activated PSCs is SMAD3-dependent.

Conclusions:

  • miR-29 plays a critical role in regulating ECM deposition by PSCs in PDAC.
  • Restoring miR-29 function in pancreatic stellate cells may represent a potential therapeutic strategy for PDAC.

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