Smad6 suppresses the growth and self-renewal of hepatic progenitor cells

J Cell Physiol. 2014 May;229(5):651-60. doi: 10.1002/jcp.24488.

Abstract

Activation of hepatic progenitor cells (HPCs) is commonly observed in chronic liver disease and Wnt/β-catenin signaling plays a crucial role in the expansion of HPCs. However, the molecular mechanisms that regulate the activation of Wnt/β-catenin signaling in the liver, especially in HPCs, remain largely elusive. Here, we reported that ectopic expression of Smad6 suppressed the proliferation and self-renewal of WB-F344 cells, a HPC cell line. Mechanistically, we found that Smad6 inhibited Wnt/β-catenin signaling through promoting the interaction of C-terminal binding protein (CtBP) with β-catenin/T-cell factor (TCF) complex to inhibit β-catenin mediated transcriptional activation in WB-F344 cells. We used siRNA targeting β-catenin to demonstrate that Wnt/β-catenin signaling was required for the proliferation and self-renewal of HPCs. Taken together, these results suggest that Smad6 is a regulatory molecule which regulates the proliferation, self-renewal and Wnt/β-catenin signaling in HPCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Proliferation
  • Gene Expression Regulation
  • Liver / cytology*
  • Liver Regeneration / physiology
  • Rats
  • Smad6 Protein / pharmacology*
  • Stem Cells / cytology
  • Stem Cells / physiology*
  • Wnt Signaling Pathway / physiology
  • beta Catenin / genetics
  • beta Catenin / metabolism

Substances

  • Smad6 Protein
  • beta Catenin