Skip to main content
. 2016 Jun 30;115(3):364–370. doi: 10.1038/bjc.2016.201

Figure 4.

Figure 4

Inhibition of RHO-GTPase attenuates 12(S)-HETE-induced MLC2 phosphorylation and CCID formation. (A) Lymph endothelial cells were pre-treated with 10 μM rhosin (RHO-GTPase inhibitor) or solvent (DMSO) for 1 h and then stimulated with 12(S)-HETE for 15 min, and relative protein phosphorylation (prot. phosph.) or protein expression (prot. expr.) was quantified by densitometry (three technical replicates). The numbers below the bar graphs refer to the respective treatment conditions indicated in the lanes of the blots. Non-targeting control (n.t.Co) was set to 1. (B) Confluent LECs were pre-treated with solvent (DMSO) or 1.3, 2.5 and 5 μM rhosin or (C) 5, 10 and 20 μM pyridone P6 (JAK inhibitor) for 30 min, and then MDA-MB231 spheroids were placed on top of LECs monolayers and co-incubated for 4 h when the areas of CCIDs were measured (27–34 replicates of three independent experiments). Error bars indicate means ±s.e.m., and asterisks significance (P<0.05; t-test or ANOVA).