Glioblastoma cell death induced by asiatic acid.

TitleGlioblastoma cell death induced by asiatic acid.
Publication TypeJournal Article
Year of Publication2006
AuthorsCho, CW, Choi, DS, Cardone, MH, Kim, CW, Sinskey, AJ, Rha, C
JournalCell Biol Toxicol
Date Published2006 Nov
KeywordsAmino Acid Chloromethyl Ketones, Antineoplastic Agents, Apoptosis, Calcium, Caspase 3, Caspase 9, Caspase Inhibitors, Cell Line, Tumor, Cell Survival, Chelating Agents, Colonic Neoplasms, Cysteine Proteinase Inhibitors, DNA Fragmentation, Dose-Response Relationship, Drug, Drug Screening Assays, Antitumor, Egtazic Acid, Glioblastoma, Humans, Membrane Potential, Mitochondrial, Necrosis, Pentacyclic Triterpenes, Triterpenes

Asiatic acid (AA), a triterpene, is known to be cytotoxic to several tumor cell lines. AA induces dose- and time-dependent cell death in U-87 MG human glioblastoma. This cell death occurs via both apoptosis and necrosis. The effect of AA may be cell type-specific as AA-induced cell death was mainly apoptotic in colon cancer RKO cells. AA-induced glioblastoma cell death is associated with decreased mitochondrial membrane potential, activation of caspase-9 and -3, and increased intracellular free Ca2+. Although treatment of glioblastoma cells with the caspase inhibitor zVAD-fmk completely abolished AA-induced caspase activation, it did not significantly block AA-induced cell death. AA-induced cell death was significantly prevented by an intracellular Ca2+ inhibitor, BAPTA/AM. Taken together, these results indicate that AA induces cell death by both apoptosis and necrosis, with Ca2+-mediated necrotic cell death predominating.

Alternate JournalCell Biol Toxicol
Citation Key85
PubMed ID16897440