May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Regulation of Transforming Growth Factor–Beta Type II Receptor Expression and Structure of Promoter Region in Human Retinoblastoma Cell Lines
Author Affiliations & Notes
  • Y. Kashiwagi
    Ocular Cellular Engineering,
    Yamagata Univ, Yamagata, Japan
  • C. Kanno
    Ophthal/Visual Science,
    Yamagata Univ, Yamagata, Japan
  • K. Horie
    Research Center for Genomic Medicine, Saitama Univ, Saitama, Japan
  • M. Inomata
    Biotechnology Research, Teikyo Univ, Yamanashi, Japan
  • T. Imamura
    Biochemistry, The JFCR Cancer Institute, Tokyo, Japan
  • T. Yamamoto
    Ocular Cellular Engineering,
    Yamagata Univ, Yamagata, Japan
  • H. Yamashita
    Ophthal/Visual Science,
    Yamagata Univ, Yamagata, Japan
  • Footnotes
    Commercial Relationships  Y. Kashiwagi, None; C. Kanno, None; K. Horie, None; M. Inomata, None; T. Imamura, None; T. Yamamoto, None; H. Yamashita, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3105. doi:
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      Y. Kashiwagi, C. Kanno, K. Horie, M. Inomata, T. Imamura, T. Yamamoto, H. Yamashita; Regulation of Transforming Growth Factor–Beta Type II Receptor Expression and Structure of Promoter Region in Human Retinoblastoma Cell Lines . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3105.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Retinoblastoma is the most common intraocular malignant tumor in Japa n. The lack of TGF–beta type II receptor (T<font face="Symbol">b</font>R–II) gene expression in retinoblas toma cell lines(Rb cells) has been reported, which may be related to the tumorig enesis. In the present study, we investigated the molecular mechanism for the la ck of T <font face="Symbol">b</font>R–II gene expression by analyzing the promoter structure. Methods:We investigated the expression of TGF– <font face="Symbol">b</font> type I (T<font face="Symbol">b</font>R–I) and type II re ceptors in 5 retinoblastoma cell lines (Y79, WERI, R51, R54, R56), which was est ablished from human retinoblastoma cases. We examined the nucleic acid sequence of the promoter region of T<font face="Symbol">b</font>R–II gene in Rb cells. We treated the Rb cells wi th 5–aza–2’–deoxycytidine(5–aza–dC) and examined the mechylation sites and the recovery in the promoter region of. The mechylation site was confirmed by the b i–sulfite treatment. Results: The examined Rb cell lines expressed T<font face="Symbol">b</font>R–I gene, but not T<font face="Symbol">b</font>R–II ge ne by RT–PCR. T<font face="Symbol">b</font>R–II gene expression was recovered by the treatment with 5–aza– dC. The methylation sites in the promoter region of T <font face="Symbol">b</font>R–II gene are not always coincident among the 5 cell lines. The Sp1 site was the only common methylation site in all the 5 Rb cell lines. Conclusions: The lack of T<font face="Symbol">b</font>R–II gene expression in Rb cells may be caused by th e methylation of Sp1 site in the promoter region. This site is speculated to re gulate the expression of T<font face="Symbol">b</font>R–II gene, and to be related to the tumorigenesis.

Keywords: retinoblastoma • growth factors/growth factor receptors • gene/expression 
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