Abstract
Wnt3a activates proliferation of fibroblasts cells via activation of both extracellular signal-regulated kinase (ERK) and Wnt/β-catenin signaling pathways. In this study, we show that the phosphatidyl inositol 3 kinases (PI3K)-Akt pathway is also involved in the Wnt3a-induced proliferation. Akt was activated within 30 min by Wnt3a in NIH3T3 cells. By Wnt3a treatment, activated Akt was transiently accumulated in nucleus although β-catenin was accumulated in the nucleus of cells in a prolonged manner. The Wnt3a-induced Akt activation was not affected by siRNA-mediated reduction of β-catenin, indicating that Wnt3a-induced Akt activation may occur independently of β-catenin. The Wnt3a-induced Akt activation was abolished by pre-treatment with PI3K inhibitor, LY294002 and Wortmanin, but not by MEK inhibitor, U0126, indicating that Wnt3a activates Akt via PI3K. The growth and proliferation induced by Wnt3a were blocked by treatments of the PI3K inhibitors. Furthermore, Wnt3a-induced proliferation was blocked by Akt siRNA. These results reveal that the PI3K-Akt pathway mediates the Wnt3a-induced growth and proliferation of NIH3T3 cells.
| Original language | English |
|---|---|
| Pages (from-to) | 511-518 |
| Number of pages | 8 |
| Journal | Cellular Signalling |
| Volume | 19 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2007 Mar 1 |
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All Science Journal Classification (ASJC) codes
- Cell Biology
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The PI3 kinase-Akt pathway mediates Wnt3a-induced proliferation. / Kim, Sung Eun; Lee, Won Jeong; Choi, Kang-Yell.
In: Cellular Signalling, Vol. 19, No. 3, 01.03.2007, p. 511-518.Research output: Contribution to journal › Article
TY - JOUR
T1 - The PI3 kinase-Akt pathway mediates Wnt3a-induced proliferation
AU - Kim, Sung Eun
AU - Lee, Won Jeong
AU - Choi, Kang-Yell
PY - 2007/3/1
Y1 - 2007/3/1
N2 - Wnt3a activates proliferation of fibroblasts cells via activation of both extracellular signal-regulated kinase (ERK) and Wnt/β-catenin signaling pathways. In this study, we show that the phosphatidyl inositol 3 kinases (PI3K)-Akt pathway is also involved in the Wnt3a-induced proliferation. Akt was activated within 30 min by Wnt3a in NIH3T3 cells. By Wnt3a treatment, activated Akt was transiently accumulated in nucleus although β-catenin was accumulated in the nucleus of cells in a prolonged manner. The Wnt3a-induced Akt activation was not affected by siRNA-mediated reduction of β-catenin, indicating that Wnt3a-induced Akt activation may occur independently of β-catenin. The Wnt3a-induced Akt activation was abolished by pre-treatment with PI3K inhibitor, LY294002 and Wortmanin, but not by MEK inhibitor, U0126, indicating that Wnt3a activates Akt via PI3K. The growth and proliferation induced by Wnt3a were blocked by treatments of the PI3K inhibitors. Furthermore, Wnt3a-induced proliferation was blocked by Akt siRNA. These results reveal that the PI3K-Akt pathway mediates the Wnt3a-induced growth and proliferation of NIH3T3 cells.
AB - Wnt3a activates proliferation of fibroblasts cells via activation of both extracellular signal-regulated kinase (ERK) and Wnt/β-catenin signaling pathways. In this study, we show that the phosphatidyl inositol 3 kinases (PI3K)-Akt pathway is also involved in the Wnt3a-induced proliferation. Akt was activated within 30 min by Wnt3a in NIH3T3 cells. By Wnt3a treatment, activated Akt was transiently accumulated in nucleus although β-catenin was accumulated in the nucleus of cells in a prolonged manner. The Wnt3a-induced Akt activation was not affected by siRNA-mediated reduction of β-catenin, indicating that Wnt3a-induced Akt activation may occur independently of β-catenin. The Wnt3a-induced Akt activation was abolished by pre-treatment with PI3K inhibitor, LY294002 and Wortmanin, but not by MEK inhibitor, U0126, indicating that Wnt3a activates Akt via PI3K. The growth and proliferation induced by Wnt3a were blocked by treatments of the PI3K inhibitors. Furthermore, Wnt3a-induced proliferation was blocked by Akt siRNA. These results reveal that the PI3K-Akt pathway mediates the Wnt3a-induced growth and proliferation of NIH3T3 cells.
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UR - http://www.scopus.com/inward/citedby.url?scp=33846256558&partnerID=8YFLogxK
U2 - 10.1016/j.cellsig.2006.08.008
DO - 10.1016/j.cellsig.2006.08.008
M3 - Article
VL - 19
SP - 511
EP - 518
JO - Cellular Signalling
JF - Cellular Signalling
SN - 0898-6568
IS - 3
ER -