Exp Mol Med.  2004 Aug;36(4):380-386.

Implication of Egr-1 in trifluoperazine-induced growth inhibition in human U87MG glioma cells

Affiliations
  • 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.

Keyword

cell cycle; cyclin D1; glioma; trifluoperazine; tumor suppressor proteins
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