Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 229, Issue 5, Pages 651-660Publisher
WILEY
DOI: 10.1002/jcp.24488
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Funding
- National Natural Science Foundation of China [30973498, 81072001]
- State Key Project on Infection Disease of China [2012ZX10002016-004, 2012ZX10002010-001-004]
- Chinese Ministry of Public Health for Key Clinical Project [[2010] 493-51]
- Graduate Practice Base of Innovation and Enterprise, Huazhong University of Science and Technology [HF-09-34-2011-540, 2011JC065]
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Activation of hepatic progenitor cells (HPCs) is commonly observed in chronic liver disease and Wnt/-catenin signaling plays a crucial role in the expansion of HPCs. However, the molecular mechanisms that regulate the activation of Wnt/-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/-catenin signaling through promoting the interaction of C-terminal binding protein (CtBP) with -catenin/T-cell factor (TCF) complex to inhibit -catenin mediated transcriptional activation in WB-F344 cells. We used siRNA targeting -catenin to demonstrate that Wnt/-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/-catenin signaling in HPCs. J. Cell. Physiol. 229: 651-660, 2014. (c) 2013 Wiley Periodicals, Inc.
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