RGD Reference Report - Activation of c-Jun N-terminal kinase 1 and caspase 3 in the tamoxifen-induced apoptosis of rat glioma cells. - Rat Genome Database

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Activation of c-Jun N-terminal kinase 1 and caspase 3 in the tamoxifen-induced apoptosis of rat glioma cells.

Authors: Tseng, SH  Wang, CH  Lin, SM  Chen, CK  Huang, HY  Chen, Y 
Citation: Tseng SH, etal., J Cancer Res Clin Oncol. 2004 May;130(5):285-93. Epub 2004 Mar 2.
RGD ID: 10412686
Pubmed: PMID:14997384   (View Abstract at PubMed)
DOI: DOI:10.1007/s00432-004-0546-y   (Journal Full-text)

PURPOSE: The mechanisms of the antitumor effects of tamoxifen upon gliomas are still unclear. In this study, we investigated the role of c-Jun N-terminal kinase-1 (JNK1) and caspase 3 in the tamoxifen-induced apoptosis of rat glioma cells. METHODS: Glioma cells were treated with tamoxifen, followed by a cytotoxicity assay to study its effects on the cells, and then a flow-activated cell sorter (FACS) analysis was performed to analyze the cellular apoptosis of the glioma cells. The expression of JNK1 and phospho-specific JNK1 in glioma cells treated with tamoxifen was investigated by Western blot analysis. The activity of caspase 3 in glioma cells was analyzed by caspase activity assay. RESULTS: Tamoxifen was demonstrated to exert cytotoxic effects upon and induced apoptosis of the glioma cells in a concentration- and time-dependent manner (P<0.05). Western blot analysis demonstrated that tamoxifen increased the expression of phospho-specific JNK1 in glioma cells, and an increasing concentration of tamoxifen induced an increasing expression of phospho-specific JNK1. Four-hour 50-microM tamoxifen treatment increased the expression of phospho-specific JNK1 to 3.2 times that of the control level in glioma cells. Tamoxifen also increased the activity of caspase 3 in glioma cells. Pretreatment of glioma cells with the antisense oligonucleotide (OGN) of JNK1 immediately prior to tamoxifen treatment suppressed the expression of phospho-specific JNK1 and the activity of caspase 3. The apoptosis fraction of glioma cells induced by 4-h treatment with 50 microM tamoxifen was decreased from 51% to 28% by pretreatment with the antisense OGN of JNK1 (P<0.003), and to 20% by pretreatment with caspase 3 inhibitor (DEVD-CHO) (P<0.0008). CONCLUSIONS: The results suggest that the tamoxifen-induced apoptosis of rat glioma cells is related to the activation of the JNK1/caspase 3 signaling pathway; however, the confirmation of the occurrence of such activation in vivo needs further investigation.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
glial cell apoptotic process  IEP 10412686 RGD 
positive regulation of glial cell apoptotic process  IMP 10412686 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mapk8  (mitogen-activated protein kinase 8)


Additional Information