SHIBATA Hiroyuki

写真a

Affiliation

Graduate School of Medicine  Doctorial Course in Medicine  Oncoregulatory Medicine  Department of Clinical Oncology

Date of Birth

1962

Laboratory Address

Hondo 1-1-1, Akita

Laboratory Phone number

+81-18-884-6261

Laboratory Fax number

+81-18-884-6455

Mail Address

E-mail address

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Research Interests 【 display / non-display 】

  • Medical Oncology

  • Molecular Oncology

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Graduating School 【 display / non-display 】

  • 　
    -
    1987.03

    Tohoku University   Faculty of Medicine   Graduated

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Graduate School 【 display / non-display 】

  • 　
    -
    1991.03

    Tohoku University  Graduate School,Division of Medicine  Doctor's Course  Completed

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Campus Career 【 display / non-display 】

  • 2022.04
    -
    Now

    Akita University   Graduate School of Medicine   Doctorial Course in Medicine   Oncoregulatory Medicine   Department of Comprehensive Cancer Control   Professor  

  • 2022.04
    -
    Now

    Akita University   Hospital   Center for Cancer Registry and Information Service   Professor  

  • 2021.04
    -
    Now

    Akita University   Graduate School of Advanced Healthcare Engineering   Professor  

  • 2009.04
    -
    Now

    Akita University   Graduate School of Medicine   Doctorial Course in Medicine   Oncoregulatory Medicine   Department of Clinical Oncology   Professor  

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Research Areas 【 display / non-display 】

  • Life Science / General internal medicine

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Thesis for a degree 【 display / non-display 】

  • Increase in the level of P-glycoprotein mRNA expression in multidrug-resistant K562 cell lines treated with sodium butyrate is not accompanied with erythroid differentiation

    Shibata H, Kanamaru R, Sato T, Ishioka C, Konishi Y, Ishikawa A, Wakui A, Tsuruo T 

    Jpn J Cancer Res.    1991.03

    Domestic Co-author

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Research Achievements 【 display / non-display 】

    ◆Original paper【 display / non-display 】

  • Curcumin affects function of Hsp90 and drug efflux pump of Candida albicans

    Yean Sheng Lee, Xinyue Chen, Tria Widiasih Widiyanto, Kanami Orihara, Hiroyuki Shibata, Susumu Kajiwara

    Frontiers in Cellular and Infection Microbiology ( Frontiers in Cellular and Infection Microbiology )  12   2022.09  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • TGF-β and Cancer Immunotherapy

    Takashi MaruYama, WanJun Chen, Hiroyuki Shibata

    Biological and Pharmaceutical Bulletin ( Biological and Pharmaceutical Bulletin )  45 ( 2 ) 155 - 161   2022.02  [Refereed]

    Research paper (journal)   International Co-author

    <p>The cytokine, transforming growth factor beta (TGF-β), has a history of more than 40 years. TGF-β is secreted by many tumor cells and is associated with tumor growth and cancer immunity. The canonical TGF-β signaling pathway, SMAD, controls both tumor metastasis and immune regulation, thereby regulating cancer immunity. TGF-β regulates multiple types of immune cells in tumor microenvironment, including T cells, natural killer (NK) cells, and macrophages. One of the main roles of TGF-β in the tumor microenvironment is the generation of regulatory T cells, which contribute to the suppression of anti-tumor immunity. Because cancer is one of the highest causes of death globally, the discovery of immune checkpoint inhibitors by Honjo and Allison in cancer immunotherapy earned a Nobel Prize in 2018. TGF-β also regulates the levels of immune checkpoints inhibitory receptors on immune cells. Immune checkpoints inhibitors are now being developed along with anti-TGF-β antibody and/or TGF-β inhibitors. More recently, chimeric antigen receptors (CARs) were applied to cancer immunity and tried to combine with TGF-β blockers.</p>

    DOI CiNii Research

  • Two Cases of ALK-Altered Cancers of Unknown Primary Diagnosed by Immunohistochemistry

    Yoriko Kato, Kazuhiro Shimazu, Koji Fukuda, Taichi Yoshida, Daiki Taguchi, Hanae Shinozaki, Hiroshi Nanjyo, Hiroyuki Shibata

    Case Reports in Oncology ( Case Reports in Oncology )  15 ( 1 ) 21 - 26   2022.01  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • A novel Lynch syndrome pedigree bearing germ-line MSH2 missense mutation c.1808A&gt;T (Asp603Val)

    Risako Sekine, Kazuhiro Shimazu, Daisuke Nakano, Tatsuro Yamaguchi, Yusato Suzuki, Koji Fukuda, Taichi Yoshida, Daiki Taguchi, Katsunori Iijima, Hiroshi Nanjyo, Hiroyuki Shibata

    Japanese journal of clinical oncology ( Japanese journal of clinical oncology )  52 ( 1 ) 81 - 85   2022.01  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

  • Clinical decisions by the molecular tumor board on comprehensive genomic profiling tests in Japan: A retrospective observational study

    Hidekazu Shirota, Keigo Komine, Masanobu Takahashi, Shin Takahashi, Eisaku Miyauchi, Hidetaka Niizuma, Hiroshi Tada, Muneaki Shimada, Tetsuya Niihori, Yoko Aoki, Ikuko Sugiyama, Maako Kawamura, Jun Yasuda, Shuhei Suzuki, Takeshi Iwaya, Motonobu Saito, Tsuyoshi Saito, Hiroyuki Shibata, Toru Furukawa, Chikashi Ishioka

    Cancer Medicine ( Cancer Medicine )  12 ( 5 ) 6170 - 6181   2022.01  [Refereed]

    Research paper (journal)   Domestic Co-author

    DOI

    • display all >>

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    ◆Other【 display / non-display 】

  • The curcumin analog, GO-Y022 suppressed the pressure overload-induced systolic dysfunction at a lower concentration than curcumin

    Yuta Hirako, Shimizu Kana, Funamoto Masahumi, Kawase Yuto, Wu Hanhao, Sunagawa Yoichi, Katanasaka Yasuhumi, Shimizu Satoshi, Shibata Hiroyuki, Hasegawa Koji, Morimoto Tatsuya

    Proceedings for Annual Meeting of The Japanese Pharmacological Society ( Japanese Pharmacological Society )  95 ( 0 ) 1-SS-34   2022

    Domestic Co-author

    <p>Background: We previously reported that natural compound curcumin suppresses cardiomyocyte hypertrophy and the development of heart failure via inhibiting p300 histone acetyltransferase (HAT) activity. In this study, we investigated the effect of curcumin analogue, GO-Y022 on p300-HAT activity, cultured cardiomyocyte hypertrophy and heart failure in vivo.</p><p>Methods &#x26; Results: In vitro HAT assay using recombinant p300-HAT domain showed that GO-Y022 inhibited p300-HAT activity as well as curcumin. Primary cultured cardiomyocytes prepared from neonatal rats were treated with curcumin or GO-Y022 and stimulated with phenylephrine (PE). 1 µM GO-Y022 suppressed the following results to the same extent as 10 µM of curcumin: PE-induced histone acetylation, hypertrophic response gene transcription, and cardiomyocyte hypertrophy. Finally, 8-week-old C57BL/6J male mice were subjected to transverse aortic constriction (TAC) surgery and orally administrated GO-Y022 or curcumin for 8 weeks. Cardiac echography indicated that a low dose of GO-Y022 (1 mg/kg) repressed TAC-induced increase in left ventricular posterior wall dimension and decrease in Fractional shortening to the same extent as 50 mg/kg of curcumin. </p><p>Conclusion: GO-Y022 may be used for heart failure therapy at a lower dose than curcumin.</p>

    DOI CiNii Research

  • The Curcumin Analogue GO-Y022 Suppresses Pressure Overload-induced Systolic Dysfunction

    Yuta Hirako, Sunagawa Yoichi, Shimizu Kana, Funamoto Masafumi, Katanasaka Yasufumi, Hamabe Toshihide, Shibata Hiroyuki, Komiyama Maki, Hasegawa Koji, Morimoto Tatsuya

    Proceedings for Annual Meeting of The Japanese Pharmacological Society ( Japanese Pharmacological Society )  96 ( 0 ) 3-B-P-214   2022

    <p><b>【Introduction】</b>We previously found that a natural p300 HAT inhibitor, curcumin (CUR), can inhibit cardiomyocyte hypertrophy and the development of heart failure <i>in vivo</i>. We focused on a CUR analog, GO-Y022, which shows stronger anti-cancer activity than CUR. The purpose of this study was to determine whether GO-Y022 inhibits p300-HAT activity and can be used as a therapeutic agent for heart failure. </p><p><b>【Methods & Results】</b><i>In vitro</i> HAT assay using recombinant p300-HAT domain showed that GO-Y022 inhibited p300-HAT activity as well as CUR. Primary cultured cardiomyocytes prepared from neonatal rats were treated with GO-Y022 or CUR and then stimulated with phenylephrine (PE) for 48 hours. One µM of GO-Y022 suppressed PE-induced histone H3K9 acetylation, hypertrophic response gene transcription, and cardiomyocyte hypertrophy to the same extent as 10 µM of CUR. C57BL/6j male mice were subjected to transverse aortic constriction (TAC) or sham operation. The TAC mice were randomly assigned to five groups: Vehicle, CUR at 1 or 50 mg/kg, or GO-Y022 at 0.2 or 1 mg/kg. After 8 weeks daily oral treatment, echocardiographic analysis showed that 1 mg/kg of GO-Y022 and 50 mg/kg of CUR improved a TAC-induced increase in left ventricular posterior wall thickness and a decrease in fractional shortening.</p><p><b>【Conclusion</b>】These results indicate that GO-Y022 strongly inhibits both PE-induced hypertrophic responses and pressure overload-induced development of heart failure. These findings suggest that GO-Y022 may be a novel candidate agent for heart failure therapy.</p>

    DOI CiNii Research

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Grant-in-Aid for Scientific Research 【 display / non-display 】

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2020.04  -  2023.03 

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2013.04  -  2016.03 

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2010.04  -  2013.03 

  • Grant-in-Aid for Scientific Research on Priority Areas

    Project Year： 2005.04  -  2010.03 

  • Grant-in-Aid for Scientific Research(C)

    Project Year： 2004.04  -  2006.03 

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Presentations 【 display / non-display 】

  • The curcumin analog, GO-Y022 suppressed the pressure overload-induced systolic dysfunction at a lower concentration than curcumin

    Yuta Hirako, Shimizu Kana, Funamoto Masahumi, Kawase Yuto, Wu Hanhao, Sunagawa Yoichi, Katanasaka Yasuhumi, Shimizu Satoshi, Shibata Hiroyuki, Hasegawa Koji, Morimoto Tatsuya

    Proceedings for Annual Meeting of The Japanese Pharmacological Society  2022  -  2022  Japanese Pharmacological Society

    <p>Background: We previously reported that natural compound curcumin suppresses cardiomyocyte hypertrophy and the development of heart failure via inhibiting p300 histone acetyltransferase (HAT) activity. In this study, we investigated the effect of curcumin analogue, GO-Y022 on p300-HAT activity, cultured cardiomyocyte hypertrophy and heart failure in vivo.</p><p>Methods &#x26; Results: In vitro HAT assay using recombinant p300-HAT domain showed that GO-Y022 inhibited p300-HAT activity as well as curcumin. Primary cultured cardiomyocytes prepared from neonatal rats were treated with curcumin or GO-Y022 and stimulated with phenylephrine (PE). 1 µM GO-Y022 suppressed the following results to the same extent as 10 µM of curcumin: PE-induced histone acetylation, hypertrophic response gene transcription, and cardiomyocyte hypertrophy. Finally, 8-week-old C57BL/6J male mice were subjected to transverse aortic constriction (TAC) surgery and orally administrated GO-Y022 or curcumin for 8 weeks. Cardiac echography indicated that a low dose of GO-Y022 (1 mg/kg) repressed TAC-induced increase in left ventricular posterior wall dimension and decrease in Fractional shortening to the same extent as 50 mg/kg of curcumin. </p><p>Conclusion: GO-Y022 may be used for heart failure therapy at a lower dose than curcumin.</p>

    DOI

  • The Curcumin Analogue GO-Y022 Suppresses Pressure Overload-induced Systolic Dysfunction

    Yuta Hirako, Sunagawa Yoichi, Shimizu Kana, Funamoto Masafumi, Katanasaka Yasufumi, Hamabe Toshihide, Shibata Hiroyuki, Komiyama Maki, Hasegawa Koji, Morimoto Tatsuya

    Proceedings for Annual Meeting of The Japanese Pharmacological Society  2022  -  2022  Japanese Pharmacological Society

    <p><b>【Introduction】</b>We previously found that a natural p300 HAT inhibitor, curcumin (CUR), can inhibit cardiomyocyte hypertrophy and the development of heart failure <i>in vivo</i>. We focused on a CUR analog, GO-Y022, which shows stronger anti-cancer activity than CUR. The purpose of this study was to determine whether GO-Y022 inhibits p300-HAT activity and can be used as a therapeutic agent for heart failure. </p><p><b>【Methods & Results】</b><i>In vitro</i> HAT assay using recombinant p300-HAT domain showed that GO-Y022 inhibited p300-HAT activity as well as CUR. Primary cultured cardiomyocytes prepared from neonatal rats were treated with GO-Y022 or CUR and then stimulated with phenylephrine (PE) for 48 hours. One µM of GO-Y022 suppressed PE-induced histone H3K9 acetylation, hypertrophic response gene transcription, and cardiomyocyte hypertrophy to the same extent as 10 µM of CUR. C57BL/6j male mice were subjected to transverse aortic constriction (TAC) or sham operation. The TAC mice were randomly assigned to five groups: Vehicle, CUR at 1 or 50 mg/kg, or GO-Y022 at 0.2 or 1 mg/kg. After 8 weeks daily oral treatment, echocardiographic analysis showed that 1 mg/kg of GO-Y022 and 50 mg/kg of CUR improved a TAC-induced increase in left ventricular posterior wall thickness and a decrease in fractional shortening.</p><p><b>【Conclusion</b>】These results indicate that GO-Y022 strongly inhibits both PE-induced hypertrophic responses and pressure overload-induced development of heart failure. These findings suggest that GO-Y022 may be a novel candidate agent for heart failure therapy.</p>

    DOI

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