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

Cited 16 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
2006-04-07
Publisher
Wiley-Blackwell
Citation
J Cell Biochem. 2006 Sep 1;99(1):88-95.
Keywords
Carcinoma/metabolism/pathologyCell Line, TumorCell Movement/*drug effects/*physiologyCofilin 1/drug effects/metabolismDose-Response Relationship, DrugEnzyme Inhibitors/pharmacologyFibronectins/metabolismFocal Adhesion Kinase 1/drug effects/metabolismHumansIntegrins/drug effects/*metabolismMolecular MimicryPaxillin/drug effects/metabolismPhosphorylationProtein Kinase C-delta/antagonists & inhibitors/metabolismProtein-Tyrosine Kinases/drug effects/metabolismStomach Neoplasms/metabolism/pathologyTetradecanoylphorbol Acetate/*pharmacologyTransforming Growth Factor beta/metabolism/pharmacologyTransforming Growth Factor beta1rhoA GTP-Binding Protein/drug effects/metabolism
Abstract
Spreading of SNU16mAd gastric carcinoma cells was previously shown to be regulated via a signaling network from transforming growth factor beta1 (TGFbeta1) to integrins signaling, through a mediation of protein kinase C delta (PKCdelta). However, in the previous study, the roles of PKCdelta appeared complicated. In this study to clarify the roles of PKCdelta in the spreading of the gastric carcinoma cells, we questioned if PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment could mimic the TGFbeta1 effects. An acute PMA treatment increased phosphorylations of focal adhesion (FA) kinase, paxillin, c-Src, and cofilin, just as TGFbeta1 did. Furthermore, cell spreading mediated by TGFbeta1- or acute PMA treatment correlated with activation of RhoA, which regulates actin reorganization and FA formation. However, stress fiber formation was prominent in TGFbeta1-treated cells, compared to cortical actin organization in PMA-treated cells. Altogether, these observations indicate that acute PMA treatment could mimic the TGFbeta1 mechanisms for cell spreading through subtly different effects on actin reorganization.
ISSN
0730-2312 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16598791

http://hdl.handle.net/10371/47143
DOI
https://doi.org/10.1002/jcb.20830
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College of Medicine/School of Medicine (의과대학/대학원)Molecular and Clinical Oncology (분자종양의학전공)Journal Papers (저널논문_분자종양의학전공)
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