• Open Access

Analysis of APCL, a Brain-specific Adenomatous Polyposis Coli Homologue, for Mutations and Expression in Brain Tumors

Authors

  • Hidewaki Nakagawa,

    1. Department of Clinical Genetics, Biomedical Research Center, Osaka University, Osaka 565-0871
    2. The 2nd Department of Surgery, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871
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  • Kumiko Koyama,

    1. Department of Clinical Genetics, Biomedical Research Center, Osaka University, Osaka 565-0871
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  • Morito Monden,

    1. The 2nd Department of Surgery, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871
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  • Yusuke Nakamura

    Corresponding author
    1. Department of Clinical Genetics, Biomedical Research Center, Osaka University, Osaka 565-0871
    2. Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639
    • To whom correspondence should be addressed at the Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo. E-mail: yusuke@ims.u-tokyo.ac.jp

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Abstract

We recently identified a novel homologue of the adenomatous polyposis coli (APC) tumor suppressor gene, APCL, whose abundant and specific expression in the central nervous system indicated an important role in neuronal proliferation and differentiation. To investigate possible involvement of APCL alterations in brain tumors, we first analyzed the expression of APCL mRNA in seven glioma tissues by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis, and in nine glioma cell lines by northern blotting. APCL expression was reduced significantly in most of the glioma tissues and all nine cell lines in comparison with normal brain tissue. However, single-strand conformation polymorphism (SSCP) analysis and DNA sequencing of the entire coding region of APCL detected no mutations in any of the glioma cell lines, or in any of the 35 astrocytic gliomas and five medulloblastomas examined. Our results suggested that some epigenetic mechanism is responsible for the decrease in APCL expression in our panel of brain tumors.

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