Molecular mechanism of trifluoperazine induces apoptosis in human A549 lung adenocarcinoma cell lines.

The mechanism by which trifluoperazine (TFP) induces apoptosis and inhibits growth in human A549 lung adenocarcinoma cells has not been entirely elucidated. In the present study, we investigated the anticancer mechanism of TFP in vitro using the human A549 lung adenocarcinoma cell line. The results indicate that TFP significantly inhibited the proliferation of A549 cells in a dose- and time-dependent manner by inducing apoptosis. Apoptotic progression in A549 cells was associated with the disruption of actin microfilaments. Moreover, the anti-apoptotic Bcl-2 protein and F-actin were down-regulated by TFP treatment, while Bax protein levels were enhanced and the phosphorylation levels of ERK and JNK proteins were increased. The data provide a potential mechanism for the chemopreventive activity of calmodulin antagonist, and suggest that TFP may have therapeutic potential for the treatment of human lung cancer.