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Integrin signaling and cell spreading mediated by phorbol 12-myristate 13-acetate treatment

Cited 17 time in Web of Science Cited 16 time in Scopus
Authors
Lee, Mi-Sook; Kim, Yong-Bae; Lee, Sung-Yul; Kim, Jeong-Geun; Kim, Sung-Hoon; Ye, Sang-Kyu; Lee, Jung Weon
Issue Date
2006-09
Publisher
Wiley-Blackwell
Citation
JOURNAL OF CELLULAR BIOCHEMISTRY Vol.99 No.1, pp. 88-95
Keywords
복합학cell spreadingintegrinRhoAPMATGFb1
Abstract
Spreading of SNU16mAd gastric carcinoma cells was previously shown to be regulated via a signaling network from transforming growth factor beta 1 (TGF beta 1) to integrins signaling, through a mediation of protein kinase C delta (PKC delta). However, in the previous study, the roles of PKC delta appeared complicated. In this study to clarify the roles of PKC delta in the spreading of the gastric carcinoma cells, we questioned if PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment could mimic the TGF beta 1 effects. An acute PMA treatment increased phosphorylations of focal adhesion (FA) kinase, paxillin, c-Src, and cofilin, just as TGF beta 1 did. Furthermore, cell spreading mediated by TGF beta 1 - or acute PMA treatment correlated with activation of RhoA, which regulates actin reorganization and FA formation. However, stress fiber formation was prominent in TGF beta 1-treated cells, compared to cortical actin organization in PMA-treated cells. Altogether, these observations indicate that acute PMA treatment could mimic the TGF beta 1 mechanisms for cell spreading through subtly different effects on actin reorganization.
ISSN
0730-2312
Language
English
URI
https://hdl.handle.net/10371/82049
DOI
https://doi.org/10.1002/jcb.20830
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College of Pharmacy (약학대학)Dept. of Pharmacy (약학과)Journal Papers (저널논문_약학과)
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