Digitoxin is a potential anticancer agent for several types of cancer.
The ability of digitalis to block cell proliferation has been well established for some time. Recently, digitalis in non-toxic concentrations has been showed to induce apoptosis in different malignant cell lines. In light of the pivotal role of apoptosis in cancer development and progression and this new experimental finding concerning digitalis, it seems probable that the apoptosis-inducing capability is explained by mechanisms other than just Na+/K+ ATPase inhibition. In this article, features of the cardiac glycosides which make them interesting to evaluate further as potential anticancer drugs are discussed. Some new data concerning inhibition and apoptosis in three human glioblastoma cell lines by digitoxin are also presented.
Haux
J
J
Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, Trondheim. Johan.Haux@medisin.ntnu.no
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D004071:Digitalis Glycosides / Q000627:therapeutic use; D004074:Digitoxin / Q000627:therapeutic use*; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D013629:Tamoxifen / Q000627:therapeutic use; D014407:Tumor Cells, Cultured
D000970:Antineoplastic Agents; D004071:Digitalis Glycosides; D004791:Enzyme Inhibitors; D013629:Tamoxifen; D004074:Digitoxin; D000254:Sodium-Potassium-Exchanging ATPase