Apoptosis induced by the sodium butyrate in human gastric cancer TMK-1 cells

The effects of sodium butyrate on cell proliferation, gene expression, and apoptosis were investigated. Upon exposure to sodium butyrate the cells exh ibited marked morphological changes, reduced cell proliferation and most ce lls died through apoptosis within 48 hours. In the presence of dexamethason e, however, the sodium butyrate-triggered apoptosis was markedly reduced. S tudies using the glucocorticoid receptor antagonist RU486 indicated that th e protective effect of dexamethasone was mediated through glucocorticoid re ceptor. Sodium butyrate markedly induced the c-jun proteins level, whereas the c-Myc protein was down-regulated rapidly. c-Jun protein may play an imp ortant role in the action of sodium butyrate since its induction preceded t he onset of DNA fragmentation. In addition preincubation of the cells with dexamethasone markedly delayed the induction of c-jun levels by sodium buty rate. Analysis of the expression of bel-2-related genes indicated that the Bcl-xS protein level was increased in the presence of sodium butyrate and t he up-regulation of Bcl-xS by sodium butyrate was also blocked by dexametha sone. Taken together these results indicate that c-myc, c-jun and Bcl-xS pr oteins may be involved in the mechanism of sodium butyrate-triggered apopto sis in these cells.