Browse

Smad2 mediates Erk1/2 activation by TGF-β1 in suspended, but not in adherent, gastric carcinoma cells

Cited 0 time in Web of Science Cited 0 time in Scopus
Authors
Lee, Mi-Sook; Ko, Seong-Gyu; Kim, Hwang-Phill; Kim, Yong-Bae; Lee, Sung-Yul; Kim, Sang-Gyun; Jong, Hyun-Soon; Kim, Tae-You; Lee, Jung Weon; Bang, Yung-Jue
Issue Date
2004-05
Citation
International Journal of Oncology, Vol.24 No.5, pp.1229-1234
Keywords
integrinTGF-beta 1erksmadcell adhesion
Abstract
Integrin-mediated cell adhesion enables cells to respond to extracellular stimuli for diverse cellular functions including proliferation, leading to differential biological activities from cells in suspension. Integrins can transduce signals (directly) to intracellular molecules and also collaborate with other membrane receptor-mediated signal pathways, including TGF-beta1 pathway. TGF-beta1 induces growth inhibition in epithelial cells and is known to transduce intracellular signaling in Smad-dependent or -independent manner. Currently effects of cell adhesion status on the TGF-beta1-mediated Erk1/2 regulation and on its Smad-(in)dependency are not known. In this study, we examined effects of cell adhesion status on the TGF-beta1-mediated Erk1/2 regulation, and roles of Smad proteins on the cell adhesion-mediated effects, using a gastric carcinoma cell variant. First, we found that cell adhesion-dependent Erk1/2 activation responded differentially to TGF-beta1, depending on cell adhesion status; TGF-beta1 treatment resulted in activation of Erk1/2 in suspended cells, whereas a decrease was noted in adherent cells. This activation of Erk1/2 by TGF-beta1 in suspension was more enhanced by an overexpression of Smad2, but not of other Smads 2, 4, and 7, but abolished by a Smad2 reduction via an introduction of its siRNA. In contrast, PKB/Akt regulation by TGF-beta1 was not different in suspension or in adhesion, and Smad7, but not the other Smads, activated PKB/Akt phosphorylation on TGF-beta1 treatment, indicating a specificity of Smad2-mediated and cell adhesion status-dependent activation of Erk1/2 activity.
ISSN
1019-6439
URI
https://hdl.handle.net/10371/173121
DOI
https://doi.org/10.3892/ijo.24.5.1229
Files in This Item:
There are no files associated with this item.
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse