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Chinese Academy of Sciences Institutional Repositories Grid
Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway

文献类型:期刊论文

作者Zhang, X; Wei, L; Yang, Y; Yu, Q
刊名JOURNAL OF CELLULAR BIOCHEMISTRY
出版日期2004-11-01
卷号93期号:4页码:819-829
ISSN号0730-2312
关键词sodium 4-phenylbutyrate JNK apoptosis lung carcinoma RNA interference
DOI10.1002/jcb.20173
文献子类Article
英文摘要Sodium 4-phenylbutyrate (PB) has been used in the therapy of urea cycle defects for many years. Recently, it has been shown to cause cellular differentiation, growth arrest, and apoptosis in certain malignancies. We have analyzed the effects of PB on human lung carcinoma cells. PB has distinct patterns of effects on different lung carcinoma cells, inducing apoptosis in NCl-H460 and NCl-H1792 cells, causing G1 arrest in A549 and SK-LU-1 cells, but having no effect on a non-transformed bronchial epithelial cell line HBE4-E6/E7. We investigated the role of MAP kinase family members, extracellular signal-regulated kinase (ERK), JNK, and p38 nitrogen-activated protein kinase (MAPK), as well as other important cell survival signaling molecules in PB-induced apoptosis. We observed activation of JNK and ERK by PB in the lung cancer cells. JNK was activated only in the two apoptotic cells, whereas ERK was activated in both the apoptotic and the growth-arrested cells, demonstrating a correlation between apoptosis and activation of JNK in response to PB. Both JNK inhibitor and JNK RNA interference (RNAi) inhibited PB-induced apoptosis, whereas MEK inhibitor did not, supporting that apoptosis induced by PB is through activation of JNK. De novo protein synthesis is required for the PB induced JNK activation and induction of apoptosis. However, the production of known upstream activators of JNK, namely Fas/Fas ligand, turner necrosis factor (TNF)-alpha, TNF-beta, and TRAIL, are not altered by PB treatment. Therefore, PB activates JNK through an unidentified and cell type-specific mechanism. Understanding of this mechanism is of therapeutic value in treating cancer patients with PB. (C) 2004 Wiley-Liss, lnc.
WOS关键词BUTYRATE-INDUCED APOPTOSIS ; BREAST-CANCER CELLS ; KAPPA-B ACTIVATION ; MEDIATED APOPTOSIS ; PROTEIN-KINASES ; INHIBITION ; ARREST ; DEATH ; P38 ; DIFFERENTIATION
资助项目NIGMS NIH HHS[R01 GM59678]
WOS研究方向Biochemistry & Molecular Biology ; Cell Biology
语种英语
出版者WILEY-LISS
WOS记录号WOS:000224933200018
源URL[http://119.78.100.183/handle/2S10ELR8/273999]  
专题中国科学院上海药物研究所
通讯作者Yu, Q
作者单位1.Boston Univ, Med Ctr, Dept Biochem, Boston, MA 02118 USA
2.Shanghai Inst Mat Med, Shanghai 201203, Peoples R China
3.Boston Univ, Med Ctr, Ctr Pulm, Dept Med, Boston, MA 02118 USA
4.Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, Guangzhou 510060, Peoples R China
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GB/T 7714
Zhang, X,Wei, L,Yang, Y,et al. Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway[J]. JOURNAL OF CELLULAR BIOCHEMISTRY,2004,93(4):819-829.
APA Zhang, X,Wei, L,Yang, Y,&Yu, Q.(2004).Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway.JOURNAL OF CELLULAR BIOCHEMISTRY,93(4),819-829.
MLA Zhang, X,et al."Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway".JOURNAL OF CELLULAR BIOCHEMISTRY 93.4(2004):819-829.

入库方式: OAI收割

来源:上海药物研究所

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