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Genes to Cells (2006) 11, 373-381. doi:10.1111/j.1365-2443.2006.00952.x
© 2006 Blackwell Publishing or its licensors
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TFII-I down-regulates a subset of estrogen-responsive genes through its interaction with an initiator element and estrogen receptor {alpha}

Yuji Ogura1, Motoki Azuma1, Yasunori Tsuboi1, Yasuaki Kabe1, Yuki Yamaguchi1, Tadashi Wada1, Hajime Watanabe2 and Hiroshi Handa1,*

1 Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259 Nagatsuta, Yokohama 226-8501, Japan
2 Okazaki Institute for Integrative Bioscience, National Institutes of Natural Sciences, Myodaiji, Okazaki, 444-8787, Japan

TFII-I was initially identified as the general transcription factor that binds to initiator (Inr) elements in vitro. Subsequent studies have shown that TFII-I activates transcription of various genes either through Inr elements or through other upstream elements in vivo. Since, however, most studies so far on TFII-I have been limited to over-expression and reporter gene assays, we reevaluated the role of TFII-I in vivo by using stable knockdown with siRNA and by examining the expression of endogenous genes. Contrary to the widely accepted view, here we show that TFII-I is not important for cell viability in general but rather inhibits the growth of MCF-7 human breast cancer cells. MCF-7 cells are known to proliferate in an estrogen-dependent manner. Through analysis of TFII-I's cell-type specific growth inhibitory effect, we show evidence that TFII-I down-regulates a subset of estrogen-responsive genes, only those containing Inr elements, by recruiting estrogen receptor (ER) {alpha} and corepressors to these promoters. Thus, this study has revealed an unexpected new role of TFII-I as a negative regulator of transcription and cell proliferation

Communicated by: Hiroshi Hamada

* Correspondence: E-mail: hhanda{at}bio.titech.ac.jp




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