Artemisinin inhibits gastric cancer cell proliferation through upregulation of p53.
Recent population studies suggest that the use of artemisinin is associated with reduced incidence and improved prognosis of certain cancers. In the current study, we assessed the effect of artemisinin on gastric cancer cells (AGS and MKN74 cells). We found that artemisinin inhibited growth and modulated expression of cell-cycle regulators in these cells. Treatment with artemisinin was also associated with induction of p27 kip1 and p21 kip1, two negative cell-cycle regulators. Furthermore, we revealed that artemisinin treatment led to an increased expression of p53. Taken together, these results provide evidence for a mechanism that may contribute to the antineoplastic effects of artemisinin suggested by recent population studies and justify further work to explore potential roles for it in gastric cancer prevention and treatment.
Hong-Tao
HT
Zhang
Yun-Long
YL
Wang
Jie
J
Zhang
Qin-Xian
QX
Zhang
D017209:Apoptosis / Q000187:drug effects; D037621:Artemisinins / Q000008:administration & dosage*; D018797:Cell Cycle Proteins; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D013274:Stomach Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics
D037621:Artemisinins; D018797:Cell Cycle Proteins; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; C031327:artemisinin