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The signaling network of transforming growth factor β1, protein kinase C delta, and integrin underlies the spreading and invasiveness of gastric carcinoma cells

Cited 37 time in Web of Science Cited 38 time in Scopus
Authors
Lee, Mi-Sook; Kim, Tae Young; Kim, Yong-Bae; Lee, Sung-Yul; Ko, Seong-Gyu; Jong, Hyun-Soon; Kim, Tae-You; Bang, Yung-Jue; Lee, Jung Weon
Issue Date
2005-08
Publisher
American Society for Microbiology
Citation
Molecular and Cellular Biology, Vol.25 No.16, pp.6921-6936
Keywords
Blotting, WesternCell AdhesionCell LineCell Line, TumorCell MovementCollagen/pharmacologyDrug CombinationsExtracellular Matrix/metabolismFibronectins/metabolismFlow CytometryFluorescent Antibody Technique, IndirectGreen Fluorescent Proteins/metabolismHumansImmunoprecipitationIntegrin alpha2/metabolismIntegrin alpha3/metabolismLaminin/pharmacologyMicroscopy, FluorescenceModels, BiologicalNeoplasm InvasivenessPhosphorylationProtein Kinase C/*metabolismProtein Kinase C-deltaProteoglycans/pharmacologyRNA, Small Interfering/metabolism*Signal TransductionStomach Neoplasms/metabolism/*pathologyTime FactorsTransfectionTransforming Growth Factor beta/*metabolismTransforming Growth Factor beta1Wound Healing
Abstract
Integrin-mediated cell adhesion and spreading enables cells to respond to extracellular stimuli for cellular functions. Using a gastric carcinoma cell line that is usually round in adhesion, we explored the mechanisms underlying the cell spreading process, separate from adhesion, and the biological consequences of the process. The cells exhibited spreading behavior through the collaboration of integrin-extracellular matrix interaction with a Smad-mediated transforming growth factor PI (TGF beta 1) pathway that is mediated by protein kinase C delta (PKC delta). TGF beta 1 treatment of the cells replated on extracellular matrix caused the expression and phosphorylation of PKC delta, which is required for expression and activation of integrins. Increased expression of integrins alpha 2 and alpha 3 correlated with the spreading, functioning in activation of focal adhesion molecules. Smad3, but not Smad2, overexpression enhanced the TGF beta 1 effects. Furthermore, TGF beta 1 treatment and PKC delta activity were required for increased motility on fibronectin and invasion through matrigel, indicating their correlation with the spreading behavior. Altogether, this study clearly evidenced that the signaling network, involving the Smad-dependent TGF beta pathway, PKC delta expression and phosphorylation, and integrin expression and activation, regulates cell spreading, motility, and invasion of the SNU16mAd gastric carcinoma cell variant.
ISSN
0270-7306
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16055706

https://hdl.handle.net/10371/47146
DOI
https://doi.org/10.1128/MCB.25.16.6921-6936.2005
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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