Gastric cancer is a common
malignancy in China, with the second highest mortality rate worldwide. Advanced
gastric cancer usually exhibits a poor prognosis with a low 5-year survival rate. Therefore, developing novel drugs for the treatment of this
cancer will be beneficial for patients.
Demethylzeylasteral, an extract of tripterygium wilfordii, has shown positive anticancer activities. However, the possible antitumor effect of
demethylzeylasteral on
gastric cancer cells and its underlying molecular mechanism remain to be determined. In the present study, the Cell Counting Kit-8 and colony formation assays revealed that
demethylzeylasteral impeded the proliferation of human
gastric cancer cells in a dose-dependent manner. Furthermore, the Transwell assay identified an inhibitory effect of
demethylzeylasteral on the migration of MKN-45 cells, while flow cytometry found that treatment with
demethylzeylasteral induced apoptosis and decreased the mitochondrial membrane potential in the
cancer cells. Further investigation revealed that
demethylzeylasteral downregulated the phosphorylation of ERK1/2, AKT, and GSK-3β in MKN-45 cells. Notably, decreased expression of Bcl-2 and increased expression of Bax, cleaved
caspase-3, cleaved
caspase-9 and cleaved PARP were detected in the
cancer cells treated with
demethylzeylasteral. The present study demonstrated that
demethylzeylasteral exhibits therapeutic potential for
gastric cancer.