Artemether suppresses cell proliferation and induces apoptosis in diffuse large B cell lymphoma cells.

Artemether (ART), a derivative of the well.known anti.malaria drug artemisinin, demonstrates potent anti.cancer activity in various cancer cells, however its effects on lymphoma remain unknown. The present study demonstrated that ART significantly inhibited proliferation of diffuse large B cell lymphoma (DLBCL) in vivo and in vitro, and led to G0/G1 phase arrest. Mechanistic studies demonstrated that ART suppressed the expression of the cell cycle proteins cyclin dependent kinase (CDK) 2, 4, and Cyclin D1, and specifically repressed the proto.oncogene c.Myc, rather than regulating the extracellular signal.regulated kinase or protein kinase B signaling pathways (two key pathways involved in regulating cell proliferation). In addition, high.concentration ART treatment significantly induced the apoptosis of DLBCL cells by promoting the cleavage of Caspase.3 and Poly (ADP.ribose) polymerase (PARP) 1. Overall, the data indicated that ART exhibited anti.cancer activity by inhibiting the expression of cell cycle genes and c.Myc, and promoting Caspase.3 and PARP1 cleavage, which suggested that ART may serve as a dual pharmaceutical for the treatment DLBCL. [ABSTRACT FROM AUTHOR]