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Researcher Information

last modified:2017/05/23

Professor TAKAHASHI Chiaki

Mail Laboratory Website
Laboratory Website

Faculty, Affiliation

Cancer Research Institute

College and School Educational Field

Division of Medical Sciences, Graduate School of Medical Science
Division of Natural Sciences, Graduate School of Natural Science and Technology
Division of Cancer Medicine, Graduate School of Medical Science
School of Medicine, College of Medical, Pharmaceutical and Health Sciences

Laboratory

Division of Oncology and Molecular Biology TEL:076-246-6750 FAX:076-234-4521

Academic Background

【Academic background(Doctoral/Master's Degree)】
Kyoto University Doctor 199603 Completed
【Academic background(Bachelor's Degree)】
Kyoto University 199003
【Degree】
MD., Ph. D.,

Career

Professor(2009/12/01-)
Associate Professor(2004/01/01-2008/03/31)
Assistant Professor(1996/06/01-2003/12/01)

Year & Month of Birth

1964/10

Academic Society







Japan Cancer Association

Award

○JFCR Young Investigators Award(2004/10)

Specialities

Pathological medical chemistry

Speciality Keywords

Molecular Oncology, Molecular Biology, Cancer Genetics

Research Themes

Molecular mechanism of tumorigenesis, progression, metastasis and cancer stem cells

Molecular mechanism of tumorigenesis, progression, metastasis and cancer stem cells We inquire the minimum requirement for inducing tumor progression and cancer stem cells. We also investigate the genetic interactions between such minimum requirements. We plan to establish in vitro cancer stem cell models that stably express various features cancer stem cells on dish. Such system would critically contribute to screen genes related to cancer stem cells or to develop drugs specifically targeting cancer stem cells.

Tumor suppressor function of RECK

Tumor suppressor function of RECK We isolated RECK gene as an antagonistic downstream target of K-rasV12. It encodes a GPI-anchored glycoprotein with multiple domains analogous to EGF, crmA and metalloendopeptidase substrates. RECK regulates Ras, beta1-integrin and Notch signaling through interaction with several soluble MMPs, MT1-MMP, ADAM10 and CD13/APN. RECK expression in various cancers significantly predicts favorable prognosis of patients. Many scientists are interested in transcriptional/post-transcriptional regulation of this gene by various oncogenic signals. We particularly focus on the cellular signals controlled by RECK.

Analysis of Rb-Ras pathway

Analysis of Rb-Ras pathway We focus on the genetic interaction of Rb and Ras in mammals. Ras regulates phosphorylation status of Rb via D-type Cyclins and CDK4/6; inversely, Rb controls isoprenylation of Ras in E2F- and SREBP-dependent manner. We found Rb-deficient carcinogenesis in thyroid C cells is antagonized by elevated N-Ras activity and subsequent DNA damage response and cellular senescence. We speculate that this Rb-Ras interaction plays critical roles in developing cancer stem cells. We are testing this hypothesis using various compound knockout mice.

tumor metabolism, microenvironment

Books

Papers

  •  ATM mediates pRB function to control DNMT1 protein stability and DNA methylation.  Shamma A, Suzuki M, Hayashi, N, Kobayashi M, Sasaki N, Nishiuchi T, Doki Y, Okamoto T, Kohno S, Muranaka H, Kitajima S, Yamamoto K, Takahashi C MOLECULAR AND CELLULAR BIOLOGY 13 10 2013/06
  •  Twists in views on RB functions in cellular signaling, metabolism and stem cells. 103 1105-1116 2012/01
  •  Rb/E2F1 regulates the innate immune receptor Toll-like receptor 3 in epithelial cells.  MOLECULAR AND CELLULAR BIOLOGY 2012/01
  •  Reversion-inducing cysteine-rich protein with Kazal motifs interferes with epidermal growth factor receptor signaling. Shunsuke Kitajama, Chiaki Takahashi et al., ONCOGENE 30 6 737-750 2011/02
  •  The beta1-integrin-dependent function of RECK in physiologic and tumor angiogenesis. Miki T, Shamma A, Kitajima S, Takegami Y, Noda M, Nakashima Y, Watanabe K, Takahashi C. Mol Cancer Res. 8 5  665-676 2010/04

show all

  •  Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. Shamma A, Takegami Y, Miki T, Kitajima S, Noda M, Obara T, Okamoto T, Takahashi C. Cancer Cell 15 4  255-269 2009/04
  •  RECK modulates Notch signaling during cortical neurogenesis by regulating ADAM10 activity. Muraguchi T, Takegami Y, Ohtsuka T, Kitajima S, Chandana EP, Omura A, Miki T, Takahashi R, Matsumoto N, Ludwig A, Noda M, Takahashi C. Nature Neuroscience 10 7  838-845 2007/07
  •  The reversion-inducing cysteine-rich protein with Kazal motifs (RECK) interacts with membrane type 1 matrix metalloproteinase and CD13/aminopeptidase N and modulates their endocytic pathways. J. Biol. Chem. 282 16  12341-12352 2007/04
  •  Nras loss induces metastatic conversion of Rb1-deficient neuroendocrine thyroid tumor. Takahashi C, Contreras B, Iwanaga T, Takegami Y, Bakker A, Bronson RT, Noda M, Loda M, Hunt JL, Ewen ME. Nature Genetics 38 1  118-123 2006/01
  •  J Biochem. 2013 Aug 5. [Epub ahead of print] Regulatory interaction between NBS1 and DNMT1 responding to DNA damage. Hayashi N, Kobayashi M, Shamma A, Morimura Y, Takahashi C, Yamamoto KI.

Conference Presentations

Arts and Fieldwork

Patent

Theme to the desired joint research

○Development of drugs targeting cancer stem cells and cancer cell metabolism.

Grant-in-Aid for Scientific Research

○「Rbがん抑制遺伝子欠失によって誘導される蛋白質高イソプレニル化の研究」(2009-2011) 

Classes (Bachelors)

Classes (Graduate Schools)

○Cancer molecular pathology 2(2017)
○Oncology and Molecular Biology(2017)
○Oncology and Molecular Biology(2017)
○Molecular Oncology(2017)
○Medical Sciences(2017)
○Cancer molecular pathology 2(2017)
○Cancer molecular pathology 2(2017)
○Oncology and Molecular Biology(2017)
○Medical Sciences(2017)
○Cancer molecular pathology 2(2017)
○Biology of Cancer 2A(2017)
○Biology of Cancer 2B(2017)
○Biology of Cancer 2B(2016)
○Biology of Cancer 2A(2016)
○Cancer molecular pathology 2(2016)
○Molecular Oncology(2016)
○Oncology and Molecular Biology(2016)
○Oncology and Molecular Biology(2016)
○Oncology and Molecular Biology(2016)

International Project

International Students

Lecture themes

Others (Social Activities)

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