Details

Autor(en) / Beteiligte

• Lu, Jin-Jian
• Meng, Ling-Hua
• Cai, Yu-Jun
• Chen, Qin
• Tong, Lin-Jiang
• Lin, Li-Ping
• Ding, Jian

Titel

Dihydroartemisinin induces apoptosis in HL-60 leukemia cells dependent of iron and p38 mitogen-activated protein kinase activation but independent of reactive oxygen species

Ist Teil von

• Cancer biology & therapy, 2008-07, Vol.7 (7), p.1017-1023

Ort / Verlag

United States: Taylor & Francis

Erscheinungsjahr

2008

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Dihydroartemisinin (DHA), the main active metabolite of artemisinin derivatives, is one of the most effective anti-malarial analogs of artemisinin. In the current study, we found that DHA inhibited the proliferation of a panel of tumor cells originated from different tissue types. DHA effectively induced apoptosis in human promyelocytic leukemia HL-60 cells, which was accompanied with mitochondrial dysfunction and caspases activation. Further studies indicated that DHA-induced apoptosis was iron-dependent. Though DHA slightly elicited superoxide anion, these reactive oxygen species (ROS) contribute little to DHA-induced apoptosis in HL-60 cells. Moreover, DHA time-dependently activated mitogen-activeted protein kinases (MAPKs) and specific inhibition of p38 MAPK, but not c-Jun-NH2-terminal kinase (JNK) or extracellular signal-regulated kinase (ERK), abolished DHA-induced apoptosis, indicating that activation of p38 MAPK is required for DHA-induced apoptosis in HL-60 cells. Altogether, our data uncover that DHA induces apoptosis is dependent of iron and p38 MAPK activation but not ROS in HL-60 cells.