alexa Inhibition of Cell Growth by Nuclear Receptor COUP-TFI: Possible Involvement of Decorin in Growth Inhibition
ISSN: 2168-9652

Biochemistry & Physiology: Open Access
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Special Issue Article

Inhibition of Cell Growth by Nuclear Receptor COUP-TFI: Possible Involvement of Decorin in Growth Inhibition

Shinji Morii1,2, Masaki Kato3, Naohiko Seki3, Natsuko Shinmen1, Katsuro Iwase1, Masaki Takiguchi1 and Takaki Hiwasa1*
1Department of Biochemistry and Genetics, Chiba University Graduate School of Medicine, Japan
2Department of Medicine and Clinical Oncology, Chiba University Graduate School of Medicine, Japan
3Department of Functional Genomics, Chiba University Graduate School of Medicine, Japan
*Corresponding Author : Takaki Hiwasa
Department of Biochemistry and Genetics
Chiba University, Graduate School of Medicine
Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Japan
Tel: +81-43-226-2541
Fax: +81-43-226-2037
E-mail: [email protected]
Received August 05, 2014; Accepted August 07, 2014; Published August 14, 2014
Citation: Morii S, Kato M, Seki N, Shinmen N, Iwase K, et al. (2014) Inhibition of Cell Growth by Nuclear Receptor COUP-TFI: Possible Involvement of Decorin in Growth Inhibition. Biochem Physiol S4:001. doi:10.4172/2168-9652.S4-001
Copyright: © 2014 Hiwasa T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The transcription factor, Chicken Ovalbumin Upstream Promoter-Transcription Factor I (COUP-TFI) is a member of the steroid/thyroid hormone receptor superfamily and plays important roles especially in development and differentiation. To investigate the effects of COUP-TFI on cell growth, we transfected this factor stably into Ha-rastransformed NIH3T3 (ras-NIH3T3) cells. Ectopic expression of COUP-TFI resulted in reduction of both proliferation rates and anchorage-independent growth. Flow cytometric analysis showed that progression through mid-S to G2/M phase was delayed in COUP-TFI transfectants. cDNA microarray analysis was performed to elucidate candidate genes whose expression levels were changed in response to COUP-TFI introduction. mRNA levels of decorin and cyclin G were elevated in COUP-TFI transfectants. Luciferase reporter assay revealed that the upstream promoter regions between –252 and -205 bp and between -204 and +42 bp of the decorin gene were responsible for COUPTFI. These suggest that decorin transactivated by COUP-TFI is one of the molecules which account for the growthinhibitory effects of COUP-TFI.

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