Exp Mol Med.
2004 Aug;36(4):380-386.
Implication of Egr-1 in trifluoperazine-induced growth inhibition in human U87MG glioma cells
- Affiliations
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- 1Institute of Natural Science and Technology, Hanyang University, Ansan Gyeonggi-do 426-791, South Korea.
- 2Division of Molecular and Life Science College of Science and Technology Hanyang University, Ansan Gyeonggi-do 426-791, South Korea younghan@hanyang.ac.kr
- 3Department of Biochemistry and Molecular Biology College of Medicine, Yeungnam University, Daegu 705-717, South Korea.
Abstract
- The early growth response gene-1 (Egr-1) is a tumor suppressor which plays an important role in cell growth, differentiation and apoptosis. Egr-1 has been shown to be down-regulated in many types of tumor tissues. Trifluoperazine (TFP), a phenothiazine class of antipsychotics, restored serum-induced Egr-1 expression in several cancer cell lines. We investigated the effect of Egr-1 expression on the TFP-induced inhibition of cell growth. Ectopic expression of Egr-1 enhanced the TFP-induced antiproliferative activity and downregulated cyclin D1 level in U87MG glioma cells. Our results suggest that antipsychotics TFP exhibits antiproliferative activity through up-regulation of Egr-1.
MeSH Terms
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Cell Cycle
Cell Proliferation/drug effects
Cyclin D1/metabolism
DNA-Binding Proteins/genetics/*metabolism
Gene Expression
Glioma/*metabolism
Humans
Immediate-Early Proteins/genetics/*metabolism
Promoter Regions (Genetics)/drug effects
Research Support, Non-U.S. Gov't
Transcription Factors/genetics/*metabolism
Trifluoperazine/*pharmacology
Tumor Cells, Cultured
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