Abstract
Spreading of SNU16mAd gastric carcinoma cells was previously shown to be regulated via a signaling network from transforming growth factor β1 (TGFβ1) to integrins signaling, through a mediation of protein kinase C δ (PKCδ). However, in the previous study, the roles of PKCδ appeared complicated. In this study to clarify the roles of PKCδ in the spreading of the gastric carcinoma cells, we questioned if PKC activation via phorbol 12‐myristate 13‐acetate (PMA) treatment could mimic the TGFβ1 effects. An acute PMA treatment increased phosphorylations of focal adhesion (FA) kinase, paxillin, c‐Src, and cofilin, just as TGFβ1 did. Furthermore, cell spreading mediated by TGFβ1‐ or acute PMA treatment correlated with activation of RhoA, which regulates actin reorganization and FA formation. However, stress fiber formation was prominent in TGFβ1‐treated cells, compared to cortical actin organization in PMA‐treated cells. Altogether, these observations indicate that acute PMA treatment could mimic the TGFβ1 mechanisms for cell spreading through subtly different effects on actin reorganization. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.