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The DNA methyltransferase inhibitor decitabine, 5-Aza-2'-deoxycytidine,possesses anti-metabolic and anticancer activities in various cancer cells. However,the biochemical mechanisms underlying decitabine-induced inhibition of invasivenessand metastasis have not been thoroughly studied. In this study, we investigatedthe effect of decitabine on the correlation between tightening of tight junctions(TJs) and anti-invasive activity in AGS human gastric cancer cells. Our data indicatedthat the inhibitory effects of decitabine on cell motility and invasiveness wereassociated with increased tightness of the TJ, which was demonstrated by an increasein transepithelial electrical resistance (TER). Immunoblotting results indicatedthat decitabine repressed the levels of the claudin proteins, major componentsof TJs that play a key role in the control and selectivity of paracellular transport.Furthermore, matrix metalloproteinase (MMP)-2 and -9 activity in the AGS cellswas dose-dependently inhibited by treatment with decitabine, and this was correlatedwith a decrease in mRNA and protein expression. In addition, these effects wererelated to inactivation of the phosphoinositide 3-kinase (PI3K)/Akt pathway inAGS cells. In conclusion, this study suggests that TJs and MMPs are critical targetsof decitabine-induced inhibition of invasiveness in AGS human gastric cancer cells.

oncology reports

Anti-invasive effects of decitabine, a DNA methyltransferase inhibitor, through tightening of tight junctions and inhibition of matrix metalloproteinase activities in AGS human gastric carcinoma cells