Implication of Egr-1 in trifluoperazine-induced growth inhibition in human U87MG glioma cells.
- Author:
Soon Young SHIN
1
;
Chang Gun KIM
;
Dong Dae HONG
;
Jung Hye KIM
;
Young Han LEE
Author Information
1. Institute of Natural Science and Technology, Hanyang University, Ansan Gyeonggi-do 426-791, South Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
cell cycle;
cyclin D1;
glioma;
trifluoperazine;
tumor suppressor proteins
- MeSH:
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
- From:Experimental & Molecular Medicine
2004;36(4):380-386
- CountryRepublic of Korea
- Language:English
-
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.
