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Kazuhiro Shiizaki

    Department of Life Sciences　Professor
    Course of Life Sciences　Professor
Last Updated :2025/05/21

Researcher Information

Degree

  • Ph.D.（2004/03）

URL

J-Global ID

Research Interests

  • cancer immune evasion   immune tolerance   Drug-metabolizing enzymes   Nuclear Receptor   環境化学物質   AhR   変異原物質   Carcinogenesis   発がん   

Research Areas

  • Environmental science/Agricultural science / Environmental effects of chemicals
  • Life sciences / Clinical pharmacy
  • Life sciences / Molecular biology

Academic & Professional Experience

  • 2024/04 - Today  Toyo UniversityFaculty of Life Sciences Department of Life SciencesAssociate Professor
  • 2020/04 - 2024/04  Toyo UniversityFaculty of Life Sciences Department of Applied Biosciences教授
  • 2015/04 - 2020/03  Toyo UniversityFaculty of Life Sciencesassociate professor
  • 2013/10 - 2015/03  独立行政法人国立がん研究センター
  • 2010/10 - 2013/09  埼玉県立がんセンター臨床腫瘍研究所
  • 2006/04 - 2010/09  大阪府立大学 産学官連携機構 遺伝子環境科学研究室
  • 2004/04 - 2006/03  (独)国立環境研究所 分子細胞毒性研究室
  • 2002/04 - 2006/03  筑波大学 人間総合科学科 博士後期課程
  • 2001/05 - 2003/04  ㈱新日本科学国立環境研究所出向
  • 1989/04 - 2001/04  ㈱ツムラ 中央研究所
  • 1988 - 1989  埼玉がんセンター生化学部実験補助員

Education

  • 2002/04 - 2006/03  University of Tsukuba  Graduate School of Comprehensive Human Sciences
  • 1983/04 - 1987/03  Saitama University  Faculty of Science  Regulation Biology

Association Memberships

  • The Japanese Environmental Mutagen and Genome Society   環境ホルモン学会   THE JAPANESE CANCER ASSOCIATION   The Japanese Environmental Mutagen Society   埼玉昆虫談話会   分子生物学会   

Published Papers

Conference Activities & Talks

MISC

Industrial Property Rights

  • 特許第5226353号:「形質転換酵母、それを用いた分析方法および分析キット」    2013/03/26
    西本幸史, 八木孝司, 川西優喜, 椎崎一宏

Awards & Honors

  • 2009 (社)近畿化学協会第9回環境技術賞
     JPN

Research Grants & Projects

  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2019/04 -2022/03 
    Author : Shiizaki Kazuhiro
     
    AhR is considered to be involved not only in xenobiotic sensors but also in immune evasion of cancer. The cecum tumorigenesis shown in AhR deficient (AhR-KO) mice is thought to be due to a breakdown in immune tolerance. Therefore, we generated double-deficient mice of RAG2 , which indicate immunodeficient mice, and inflammatory cytokine IL-6. The RAG2/AhR double-deficient mice did not develop cecum tumor, while IL-6/AhR double-deficient mice did. Kynurenine, which is involved in immune tolerance, is produced by the rate-limiting enzyme IDO, which is transcriptionally regulated by AhR. We generated an AhR-deficient cell line derived from B16F10 melanoma cells and tested it in mice. In tumor-bearing experiments, AhR knockout B16F10 cells significantly reduced the number of metastatic lesions.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2015/04 -2018/03 
    Author : Shiizaki Kazuhiro; TOTSUKA Yukari
     
    It is well documented that DNA adducts are associated with carcinogenesis. The 3rd generation of sequencing technology will enable us to determine formation of adducts on DNA molecule. We synthesized an oligonucleotide harboring one base of DNA-adduct, and performed sequencing analysis. Polymerase elongation delay was observed at the site of DNA adducts. Next, we enriched DNA fragments including adducts by using immuno-precipitation method because the amount of DNA adducts occurring in the genomic DNA was limited. By combining these methods, the relationship between adduct formation and mutations at critical positions would be clarified.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2011 -2013 
    Author : SHIIZAKI Kazuhiro; IKUTA Togo; KAWAJIRI Kaname
     
    It was reported that beta-catenin, which plays a critical role in the development of colorectal cancer, was degraded by aryl hydrocarbon receptor (AhR) in a ligand dependent manner. Confirmatory experiments of the relationship between AhR and beta-catenin were carried out in various colon cancer cell lines, but the beta-catenin degradation by AhR ligand treatment could not be observed. Furthermore, reporter assay and two-hybrid assay failed to identify the interaction between beta-catenin, CUL4B, and AhR. On the other hand, the spontaneous tumorigenesis in AhR-deficient mouse cecum was reconfirmed. It was speculated that some kind of ligand activated AhR and prevented tumorigenesis in cecum. The AhR ligand-like activities were detected in cecal contents of wild-type mice by using improved yeast reporter assay system. By the HPLC analysis, AhR ligand-like activity was found in several fractions.

Committee Membership

  • 2018/01 - Today   The Japanese Environmental Mutagen and Genome Society (JEMS)   associate editor
  • 2019/01 -2022/12   The Japanese Environmental Mutagen and Genome Society (JEMS)   Second Editorial Committee

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