Updated on 2022/08/24

写真a

 
MISHIRO Emi
 
Organization
Institute of Transformative Bio-Molecules Designated lecturer
Title
Designated lecturer
Other name(s)
MISHIRO-SATO Emi
External link

Degree 1

  1. PhD (Agriculture) ( 2007.3   Kagoshima University ) 

Research Interests 1

  1. proteomics

Research Areas 1

  1. Life Science / Applied biochemistry

Research History 3

  1. Nagoya University   Institute of Transformative Bio-Molecules

    2022.2

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    Country:Japan

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  2. Aichi Cancer Center, Research Institute

    2021.4 - 2022.1

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  3. Aichi Cancer Center, Research Institute

    2017.4 - 2021.3

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Professional Memberships 3

  1. 日本質量分析学会

    2021

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  2. 日本癌学会

    2018

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  3. 日本プロテオーム学会

    2008

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Papers 1

  1. Silencing of SmgGDS, a Novel mTORC1 Inducer That Binds to RHEBs, Inhibits Malignant Mesothelioma Cell Proliferation. International journal

    Tatsuhiro Sato, Satomi Mukai, Haruna Ikeda, Emi Mishiro-Sato, Ken Akao, Toshiyuki Kobayashi, Okio Hino, Wataru Shimono, Yoshio Shibagaki, Seisuke Hattori, Yoshitaka Sekido

    Molecular cancer research : MCR   Vol. 19 ( 5 ) page: 921 - 931   2021.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    Malignant mesothelioma (MM) is an aggressive tumor that typically develops after a long latency following asbestos exposure. Although mechanistic target of rapamycin complex 1 (mTORC1) activation enhances MM cell growth, the mTORC1 inhibitor everolimus has shown limited efficacy in clinical trials of MM patients. We explored the mechanism underlying mTORC1 activation in MM cells and its effects on cell proliferation and progression. Analysis of the expression profiles of 87 MMs from The Cancer Genome Atlas revealed that 40 samples (46%) displayed altered expression of RPTOR (mTORC1 component) and genes immediately upstream that activate mTORC1. Among them, we focused on RHEB and RHEBL1, which encode direct activators of mTORC1. Exogenous RHEBL1 expression enhanced MM cell growth, indicating that RHEB-mTORC1 signaling acts as a pro-oncogenic cascade. We investigated molecules that directly activate RHEBs, identifying SmgGDS as a novel RHEB-binding protein. SmgGDS knockdown reduced mTORC1 activation and inhibited the proliferation of MM cells with mTORC1 activation. Interestingly, SmgGDS displayed high binding affinity with inactive GDP-bound RHEBL1, and its knockdown reduced cytosolic RHEBL1 without affecting its activation. These findings suggest that SmgGDS retains GDP-bound RHEBs in the cytosol, whereas GTP-bound RHEBs are localized on intracellular membranes to promote mTORC1 activation. We revealed a novel role for SmgGDS in the RHEB-mTORC1 pathway and its potential as a therapeutic target in MM with aberrant mTORC1 activation. IMPLICATIONS: Our data showing that SmgGDS regulates RHEB localization to activate mTORC1 indicate that SmgGDS can be used as a new therapeutic target for MM exhibiting mTORC1 activation.

    DOI: 10.1158/1541-7786.MCR-20-0637

    Web of Science

    PubMed

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KAKENHI (Grants-in-Aid for Scientific Research) 5

  1. Molecular mechanisms that maintain stemness in metastatic colorectal cancer

    Grant number:22H02909  2022.4 - 2025.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

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    Authorship:Coinvestigator(s) 

  2. The role and molecular mechanism of NAT10, an RNA-modifying enzyme, in colorectal cancer.

    Grant number:22K07201  2022.4 - 2025.3

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

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    Authorship:Principal investigator 

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

  3. 臨床応用を指向したがん悪液質病態解明

    Grant number:21K07140  2021.4 - 2024.3

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    小島 康, 三城 恵美, 佐藤恵美

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    Authorship:Coinvestigator(s) 

    がん悪液質は、体重減少・骨格筋萎縮・食思不振を主徴とする臨床症候群である。進行がん患者の約8割が、悪液質を発症し、世界では年間900万人近くのがん患者が悪液質を発症していると推定されている。現在、悪液質の本態は不明で、実効性のある早期診断方法や治療介入法が存在しない。本研究では、悪液質モデル動物および臨床検体を組み合わせ、総合的に解析して悪液質治療薬の開発基盤を構築する。

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  4. Analysis of novel post-translational modifications in colorectal cancer

    Grant number:19K07656  2019.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

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    Authorship:Principal investigator 

    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

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  5. Molecular mechanisms and preventive/therapeutic targets of colon cancer metastasis

    Grant number:18H02686  2018.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

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    Authorship:Coinvestigator(s) 

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