Hepatocyte growth factor (HGF) is up-regulated in tissue repair and has been 
implicated in playing a role in this process through its anti-apoptotic and 
proliferative activities. Cyclooxygenase-2 (COX-2) is an inducible enzyme in the 
biosynthetic pathway of prostaglandins, and its activation has been shown to 
play an important role in cell growth. We previously reported that HGF 
significantly inhibited anoikis, possibly through the up-regulation of COX-2 
expression in the endometrial RL95-2 cancer cell line. Here, we report that i) 
treatment of RL95-2 cells with HGF resulted in phosphorylation of the HGF 
receptor c-Met, activation of Akt and IκB, translocation of NF-κB into the 
nucleus, and up-regulation of COX-2 mRNA; ii) the IκB-α phosphorylation 
inhibitor BAY11-7082 and the selective COX-2 inhibitor CAY10452 blocked 
HGF-mediated anoikis resistance in RL95-2 cells; and iii) HGF induced migration 
and invasion in RL95-2 cells, while the phosphatidylinositol 3-kinase (PI3K) 
inhibitor LY294002 and CAY10452 blocked these effects of HGF stimulation. Our 
data suggest that HGF possesses chemotactic ability, has anti-apoptosis action, 
and induces cellular infiltration via the PI3K/Akt pathway; it also triggers 
NF-κB activation and up-regulates COX-2 gene expression in endometrial cancer 
cells.