Triptonide blocks Wnt/β-catenin signaling via C-terminal transactivation domain of β-catenin, and promots apoptosis in Wnt-dependent cancer cells. Triptonide potently inhibits the proliferation of human B-lymphoma Raji and T-lymphoma Jurkat cells with IC 50 of 5.7 nM and 4.8 nM, respectively. Triptonide (2.5-10 nM; 6 days) significantly suppresses B-lymphoma cell colony-forming capability. Triptonide (20 nM; 3 days) promotes apoptosis through activation of PARP and caspase 3, but reduction of BCL2 protein levels in the lymphoma cells. Triptonide (5-10 nM; 72 hours) markedly reduces both total and phosphorylated Lyn proteins, and diminishes Lyn downstream ERK and ATK signal pathways.
Cell Proliferation Assay
Apoptosis Analysis
Western Blot Analysis
RT-PCR
Triptonide (5 mg/kg; i.p.; daily; for 34 days) exerts a strong anti-lymphoma effect in mice.