Dihydroartemisinin induces apoptosis in human gastric cancer cell line BGC-823 through activation of JNK1/2 and p38 MAPK signaling pathways.

摘要: Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, is associated with broad range biological properties including antitumor activity. However, the effect DHA on gastric cancer has not been clearly clarified. The aim this study was to investigate role and mechanism in human cell line BGC-823. Cell viability assessed by MTT assay. apoptosis analyzed flow cytometry. expressions extracellular signal-regulated kinase (ERK), c-Jun N-terminal (JNK), p38 mitogen-activated protein (p38 MAPK) their phosphorylated forms as well related proteins were examined western blot analysis. results demonstrated that inhibited BGC-823 cells dose- time-dependent manner. treatment upregulated expression Bax, cleaved caspase-3 -9, degraded form PARP, downregulated Bcl-2 Bcl-2/Bax ratio. Meanwhile, increased phosphorylation ERK1/2, JNK1/2 MAPK. Synthetic inhibitors or MAPK activity, but inhibitor significantly abolished DHA-induced activation -9. In vivo tumor-suppression assay further indicated displayed significant inhibitory xenografts tumor growth. These indicate induces through signaling pathways could serve potential additional chemotherapeutic agent for cancer.