Matsuzaki, Yuriko



School of Medicine, Institute for Advanced Medical Research (Division of Gene Regulation) (Shinanomachi)


Research Associate/Assistant Professor/Instructor

E-mail Address

E-mail address

External Links

Academic Background 【 Display / hide

  • 1981.04

    Tokyo Metropolitan University, Science, Biology

    Japan, Graduate School, Completed, Master's course

Academic Degrees 【 Display / hide

  • 理学博士, 東京都立大学, Dissertation



Research Areas 【 Display / hide

  • Tumor biology

Research Keywords 【 Display / hide

  • tumor medaka

Research Themes 【 Display / hide

  • Establishment of disease model using medaka, 



Books 【 Display / hide

  • 最新医学

    '松崎ゆり子, 河上裕', 2003.09

    Scope: 287-294

Papers 【 Display / hide

  • Establishment of pten knockout medaka with transcription activator–like effector nucleases (TALENs) as a model of PTEN deficiency disease

    Yuriko Matsuzaki, Tetsushi Sakuma, Takashi Yamamoto and Hideyuki Saya

    PLoS One 12 ( 10 )  2017.10

    Research paper (scientific journal), Joint Work, Accepted

     View Summary

    Phosphatase and tensin homolog (PTEN) is a lipid and protein phosphatase that antagonizes signaling by the phosphatidylinositol 3-kinase (PI3K)±AKT signaling pathway. The PTEN gene is a major tumor suppressor, with mutations of this gene occurring frequently in tumors of humans and mice. We have now developed mutant medaka deficient in PTEN with the use of transcription activator±like effector nuclease (TALEN) technology. Medaka possesses two pten genes, ptena and ptenb, similar to zebrafish. We established 16 ptena mutant lines and two ptenb mutant lines. Homozygous single pten mutants were found to be viable and fertile. In contrast, pten double-knockout (dko) embryos manifested severe abnormalities in vasculogenesis, eye size, and tail development at 72 hours post fertilization (hpf) and died before hatching. Immunoblot analysis revealed that the ratio of phosphorylated to total forms of AKT (pAKT/AKT) in pten dko embryos was four times that in wild-type embryos, indicative of up-regulation of signaling by the PI3K-AKT pathway. Treatment of pten dko embryos with the PI3K inhibitor LY294002 reduced the pAKT/AKT ratio by about
    one-half and partially rescued the defect in vasculogenesis. Additional inhibitors of the PI3K-AKT pathway, including rapamycin and N-α-tosyl-L-phenylalanyl chloromethyl ketone, also partially restored vasculogenesis in the dko embryos. Our model system thus allows pten dko embryos to be readily distinguished from wild-type embryos at an early stage of
    development and is suitable for the screening of drugs able to compensate for PTEN deficiency.

  • Establishment of HRASG12V Transgenic Medaka as a Stable Tumor Model for In Vivo Screening of Anticancer Drugs

    Matsuzaki Yuriko, Hosokai Haru, Mizuguchi Yukiyo, Fukamachi Shoji, Shimizu Atsushi, Saya Hideyuki

    PLoS ONE 8 ( 1 )  2013.01

    Research paper (scientific journal), Joint Work, Accepted

     View Summary

    <p>Most targeted anticancer drugs have been identified by screening at the molecular or cellular level in vitro. However, many compounds selected by such costly and time-consuming screening do not prove effective against tumors in vivo. The development of anticancer drugs would thus be facilitated by the availability of an in vivo screening system based on a multicellular organism. We have now established a transgenic line of the freshwater fish medaka in which melanophores (melanocytes) proliferate in a manner dependent on heat shock-induced signaling by a human RAS oncoprotein. The human HRASG12V oncogene was expressed under the control of a melanophore-specific gene promoter in order to allow visualization of tumor growth in live fish maintained in a water tank. The expression of HRASG12V was induced as a result of Cre-mediated recombination by exposure of the fish to a temperature of 37°C for 30 min, given that the Cre gene was placed under the control of a medaka heat shock promoter. One of the stable transgenic lines developed abnormal pigment cell proliferation in the eyes and epidermis with 100% penetrance by 6 months postfertilization. Sorafenib, an inhibitor of RAS signaling, was administered to the transgenic fish and was found both to reduce the extent of melanophore proliferation and to improve survival. The transgenic medaka established here thus represents a promising in vivo system with which to screen potential anticancer drugs that target RAS signaling, and this system can readily be adapted for the screening of agents that target other oncogenes. © 2013 Matsuzaki et al.</p>

  • Reversible whole-organism cell cycle arrest in a living vertebrate

    Sampetrean Oltea, Lida Shin Ichi, Makino Shinji, Matsuzaki Yuriko, Ohno Kikuo, Saya Hideyuki

    Cell Cycle 8 ( 4 ) 620 - 627 2009.02

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  1538-4101

     View Summary

    <p>In vivo cell cycle analysis in higher eukaryotes has been limited by the challenge of preserving the integrity of the living organism while visualizing dividing cells. Japanese medaka in order to visualize and manipulate the cell cycle progression in a live vertebrate. Our stable transgenic histone H2B-GFP medaka line allows fluorescence-based monitoring of the chromosomes. The system has a high specificity, with a strong GFP signal labeling the chromatin architecture. The subcellular resolution ensures detection of both normal and abnormal divisions in live recordings. This translates into the possibility to quantify temporal and spatial aspects of the cell cycle, such as length or nuclear size, as well as to expose drug toxicity at the earliest stage. We also show that acclimation to cold, a prominent feature of the eurytherm medaka, is a valuable natural way of inducing a reversible cell cycle arrest in the entire living organism. Our results suggest that this manipulation can be performed from the early stages of development, has no toxicity and does not alter the cell cycle profile of the embryo. © 2009 Landes Bioscience.</p>

  • A new melanoma antigen FABP7 is a potential target for diagnosis, immunotherapy, and molecular target therapy

    Goto, Y., Matsuzaki, Y., Murata, H., Takata, M., Aburatani, H., Hoon, D., Saida, T., Kawakami, Y.


    Research paper (scientific journal), Joint Work, Accepted,  ISSN  0022-202X

  • Identification of a novel cancer-testis antigen calreticulin2 (CRT2) frequently expressed in melanoma

    Yaguchi, Tomonori, Hayashi, Emiko, Hasegawa, Go, Fujita, Tomonobu, Kageshita, Toshiro, Sano, Makoto, Matsuzaki, Yuriko, Kawakami, Yutaka

    Pigment Cell & Melanoma Research 21 ( 2 ) 272 - 273 2008.04

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  1755-1471

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Papers, etc., Registered in KOARA 【 Display / hide

Presentations 【 Display / hide

  • PTEN knockout medaka produced by the gene editing technology and its application to screen anticancer drugs

    Yuriko Matsuzaki and Hideyuki Saya

    第76回日本癌学会学術総会, 2017.09, Symposium, Workshop, Panelist (public offering)

  • PTEN knockout medaka: analysis of the mutated phenotype detected in embryos and its application as a disease model

    Yuriko Matsuzaki, Tetsushi Sakuma, Takashi Yamamoto and Hideyuki Saya

    第39回日本分子生物学会年会, 2016.11, Poster (general)

  • Development of genetically engineered medaka tumor models for in vivo drug screening

    Yuriko Matsuzaki Hideyuki Saya

    第74回日本癌学会学術総会, 2015.10, Symposium, Workshop, Panelist (nomination)

  • Development of the PTEN knockout medaka embryos by targeted mutagenesis using transcription activator-like effector nucleases (TALENs)

    Yuriko Matsuzaki, Tetsushi Sakuma, Takashi Yamamoto and Hideyuki Saya

    第37回日本分子生物学会年会, 2014.11, Symposium, Workshop, Panelist (public offering)

  • Establishment of transgenic HRAS medaka as a tumor model for in vivo drug screening

    Yuriko Matsuzaki and Hideyuki Saya

    第73回日本癌学会学術総会, 2014.09, Oral Presentation(general)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • メダカHRAS悪性黒色腫モデルを用いた薬剤スクリーニング系の構築


    Grant-in-Aid for Scientific Research, 松崎ゆり子, Research grant, Principal Investigator

  • 遺伝子改変メダカを用いた悪性黒色腫モデル系の構築


    Grant-in-Aid for Scientific Research, 松崎ゆり子, Research grant, Principal Investigator

  • 遺伝子改変メダカを用いた分裂異常に基づく発癌モデルの構築


    Grant-in-Aid for Scientific Research, 佐谷秀行, Research grant, Co-investigator

  • 網羅的発現解析で同定した悪性黒色腫高発現遺伝子と病態解析と診断・治療への応用


    Grant-in-Aid for Scientific Research, Research grant, Principal Investigator

  • DNAチップで同定した悪性黒色腫高発現分子のRNA干渉法による病態解析と臨床応用


    Grant-in-Aid for Scientific Research, 松崎ゆり子, Research grant, Principal Investigator

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Educational Activities and Special Notes 【 Display / hide

  • 卒業研究生、大学院生の実験研究の指導および発表、論文作成指導


    , Lecture at Education Method and Practice


Social Activities 【 Display / hide

  • 国立科学博物館サイエンスコミュニケータ養成講座1受講及び修了


     View Summary


Memberships in Academic Societies 【 Display / hide

  • 日本癌学会