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

被引：25

作者：

Chen, Qingyong ^{[1
,2
]}

Wu, Li Jun ^{[1
]}

Wu, Yu Quan ^{[1
]}

Lu, Guo Hua ^{[2
]}

Jiang, Zhong Yong ^{[1
]}

Zhan, Jian Wei ^{[1
]}

Jie, Yan ^{[1
]}

Zhou, Jian Ying ^{[2
]}

机构：

[1] 117th Hosp PLA, Dept Resp Dis, Hangzhou 310013, Zhejiang, Peoples R China

[2] Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Resp Dis, Hangzhou 310003, Zhejiang, Peoples R China

来源：

MOLECULAR MEDICINE REPORTS | 2009年 / 2卷 / 05期

关键词：

trifluoperazine; apoptosis; lung adenocarcinoma cell line; actin cytoskeleton; Bcl-2; family; MAPK family; PROTEIN-KINASE; CANCER; DEATH; CYTOSKELETON; INHIBITION; MODULATION; INDUCTION; STRESS;

D O I：

10.3892/mmr_00000177

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：811 / 817

页数：7

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