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Integrin Signaling and Cell Spreading Mediated by Phorbol 12-Myristate 13-Acetate Treatment

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Authors
Lee, Jung Weon; Lee, Mi-Sook; Kim, Yong-Bae; Lee, Sung-Yul; Kim, Jeong-Geun; Kim, Sung-Hoon; Ye, Sang-Kyu
Issue Date
2006
Publisher
John Wiley & Sons
Citation
J. Cell. Biochem. 99: 88–95, 2006.
Keywords
cell spreading; integrin; RhoA; PMA; TGFb1
Abstract
Spreading of SNU16mAd gastric carcinoma cells was previously shown to be regulated via a signaling network from transforming growth factor b1 (TGFb1) to integrins signaling, through a mediation of protein kinase Cd(PKCd). However, in the previous study, the roles of PKCd appeared complicated. In this study to clarify the roles of PKCd in the spreading of the gastric carcinoma cells, we questioned if PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment could mimic the TGFb1 effects. An acute PMA treatment increased phosphorylations of focal adhesion (FA) kinase, paxillin, c-Src, and cofilin, just as TGFb1 did. Furthermore, cell spreading mediated by TGFb1- or acute PMA treatment correlated with activation of RhoA, which regulates actin reorganization and FA formation. However, stress fiber formation was prominent in TGFb1-treated cells, compared to cortical actin organization in PMA-treated cells. Altogether, these observations indicate that acute PMA treatment could mimic the TGFb1 mechanisms for cell spreading through subtly different effects on actin reorganization.
ISSN
0730-2312
Language
English
URI
http://hdl.handle.net/10371/3235
DOI
https://doi.org/10.1002/jcb.20830
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Medicine (의학과)Journal Papers (저널논문_의학과)
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