Focal adhesion kinase: Important to prostaglandin E2-mediated adhesion, migration and invasion in hepatocellular carcinoma cells

Prostaglandin E-2 has been implicated in cell growth and metastasis in many types of cancers. However, the effects of PGE(2) and its mechanism on cell adhesion, migration, and invasion have not been clarified yet. In this study, we found PGE(2) treatment significantly increased the cell adhesion, migration, and invasion in hepatocellular carcinoma (HCC) cells. In addition, the effects of PGE(2) were found to be associated with focal adhesion kinase (FAK). PGE(2) treatment increased the phosphorylation and synthesis of FAK in a (lose-dependent manner. RNA interference targeting FAK suppressed PGE(2)-mediated cell adhesion and migration. Furthermore, the downstream proteins of FAK, paxillin and Erk2, were also activated by PGE(2). PGE(2) treatment increased the phosphorylation and synthesis of paxillin in a dose-dependent manner. PGE(2) treatment also induced the phosphorylation of Erk2. PD98059, the specific inhibitor of MEK, suppressed PGE(2)-mediated cell adhesion and migration. However, it had no effect oil PGE(2)-induced activation and synthesis of FAK. These results demonstrated that PGE(2) greatly induced HCC cell adhesion, migration, and invasion by activating FAK/paxillin/Erk pathway.