Arsenic trioxide regulates gastric cancer cell apoptosis by mediating cAMP.

OBJECTIVE

Gastric cancer is a common digestive tract tumor in clinic with increasing incidence. It is suggested that arsenic trioxide (As2O3) has an inhibitory effect on many kinds of digestive system tumors. This study evaluated the impact of As2O3 on the apoptosis of gastric cancer BGC-823 cells, and analyzed its relationship with cyclic adenosine monophosphate (cAMP).

MATERIALS AND METHODS

Gastric cancer cell BGC-823 was intervened by different concentrations of As2O3 at 4 ng/ml, 8 ng/ml, and 16 ng/ml, respectively. BGC-823 cell apoptosis was evaluated by TUNEL assay. Cell cycle was determined by flow cytometry. cAMP and protein kinase C (PKC) was detected by radioimmunoassay. Apoptosis-related protein levels were tested by Western blot.

RESULTS

Compared with normal control, As2O3 significantly increased BGC-823 cell apoptosis, blocked cell cycle in G0/G1 phase, elevated cAMP and Bax level, as well as downregulated PKC, Bcl-2 and Survivin expression (p < 0.05).

CONCLUSIONS

As2O3 induced BGC-823 cell apoptosis through the up-regulation of the cAMP level and the decrease of the PKC level.