Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 232, Issue 5, Pages 1104-1113Publisher
WILEY
DOI: 10.1002/jcp.25572
Keywords
-
Categories
Funding
- Basic Science Research Programme of the National Research Foundation of Korea (NRF) [NRF-2015R1D1A1A01060393, NRF-2016R1A4A1010115]
- Hallym University [HRF-S-5-1]
Ask authors/readers for more resources
In canonical pathway, Wnt3A has been known to stabilize beta-catenin through the dissociation between beta-catenin and glycogen synthase kinase-3 beta (GSK-3 beta) that suppresses the phosphorylation and degradation of beta-catenin. In non-canonical signaling pathway, Wnt was known to activate Rho GTPases and to induce cell migration. The cross-talk between canonical and non-canonical pathways by Wnt signaling; however, has not been fully elucidated. Here, we revealed that Wnt3A induces not only the phosphorylation of GSK-3 beta and accumulation of beta-catenin but also RhoA activation in RAW264.7 and HEK293 cells. Notably, sh-RhoA and Tat-C3 abolished both the phosphorylation of GSK-3 beta and accumulation of beta-catenin. Y27632, an inhibitor of Rho-associated coiled coil kinase (ROCK) and siROCK inhibited both GSK-3 beta phosphorylation and beta-catenin accumulation. Furthermore, active domain of ROCK directly phosphorylated the purified recombinant GSK-3 beta in vitro. In addition, Wnt3A-induced cell proliferation and migration, which were inhibited by Tat-C3 and Y27632. Taken together, we propose the cross-talk between canonical and non-canonical signaling pathways of Wnt3A, which induces GSK-3 beta phosphorylation and beta-catenin accumulation through RhoA and ROCK activation. (C) 2016 Wiley Periodicals, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available