Dehydroartemisinin (DHA) is an effective anti-malaria agent. Fortilin is an anti-apoptotic molecule overexpressed in many human cancers. Here, we show that DHA binds human fortilin, increases the ubiquitination of fortilin, shortens fortilin's half-life in a proteasome-dependent fashion, and reduces cellular levels of fortilin in varieties of cells. DHA induced DNA fragmentation in U2OS cells in a fortilin-dependent manner. The fortilin-knocked-down cells were less susceptible-and fortilin-overexpressing cells more susceptible-to DHA than were wild-type cells, suggesting that apoptotic effects of DHA are-at least partly-conferred through fortilin. Together, these data suggest that fortilin is a molecular target of DHA. DHA and its derivative may prove to be viable anti-cancer agents in fortilin-overexpressing cancers. © 2008 Federation of European Biochemical Societies.
CITATION STYLE
Fujita, T., Felix, K., Pinkaew, D., Hutadilok-Towatana, N., Liu, Z., & Fujise, K. (2008). Human fortilin is a molecular target of dihydroartemisinin. FEBS Letters, 582(7), 1055–1060. https://doi.org/10.1016/j.febslet.2008.02.055
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