Fig. 3: RhoA is necessary for gastrin-stimulated paxillin tyrosine phosphorylation, cell polarization, and FA formation.

PANC-1 cancer cells were pre-treated with Rhosin, an effective inhibitor of RhoA, for 24 h and were then incubated with gastrin for 1 h. a The gastrin-stimulated and endogenous activation of RhoA was significantly inhibited by Rhosin. b Rhosin pre-treatment suppressed the tyrosine phosphorylation of paxillin that was activated by gastrin. c The images indicate increased paxillin-labeled focal adhesion formation and aggregation at the cell leading-edge stimulated by gastrin, and Rhosin pre-treatment inhibited these changes. Boxed regions indicate the area of the merged image used for the zoom. White arrows show the focal adhesion formation and aggregation at the leading edge of cells. d The histogram indicates the mean number of focal adhesions labeled by paxillin per cell. The average number of focal adhesions from a minimum of 20 cells was calculated. e, f The scratched wound healing assay (e) and Boyden invasion assay (f) were performed to show the migration and invasion of PANC-1 cells. Values are represented as the means ± SD from three independent experiments. *P < 0.05