Ishikawa Chie

写真a

Title

Assistant Professor

Researcher Number(JSPS Kakenhi)

90542358
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Current Affiliation Organization 【 display / non-display 】

  • Duty   University of the Ryukyus   Organization for Research Promotion   Assistant Professor  

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External Career 【 display / non-display 】

  • 2008.04
    -
    2008.12

    Research Fellowships of the Japan Society for the Promotion of Science  

  • 2009.01
    -
    2013.03

    University of the Ryukyus, Transdisciplinary Research Organization for Subtropics and Island Studies, Assistant Professor  

  • 2013.04
    　
    　

    Transdisciplinary Research Organization for Subtropics and Island Studies  

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Affiliated academic organizations 【 display / non-display 】

  • 2005.04
    -
    Now
     

    Japanese Cancer Association 

  • 2005.04
    -
    Now
     

    The Japanese Society For Virology 

  • 2011.04
    -
    Now
     

    Japananese Society of Hematology 

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Research Interests 【 display / non-display 】

  • oncogenic virus

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Research Areas 【 display / non-display 】

  • Life Science / Immunology

  • Life Science / Molecular biology

  • Life Science / Hematology and medical oncology

  • Life Science / Virology

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Published Papers 【 display / non-display 】

  • Importin β1 regulates cell growth and survival during adult T cell leukemia/lymphoma therapy.

    Ishikawa C, Senba M, Mori N

    Investigational new drugs ( Investigational New Drugs )    2020.09 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • The anti-malaria agent artesunate exhibits cytotoxic effects in primary effusion lymphoma.

    Ishikawa C, Mori N

    Investigational new drugs ( Investigational New Drugs )    2020.09 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • The role of CUDC-907, a dual phosphoinositide-3 kinase and histone deacetylase inhibitor, in inhibiting proliferation of adult T-cell leukemia.

    Ishikawa C, Mori N

    European journal of haematology ( European Journal of Haematology )    2020.08 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • MALT-1 as a novel therapeutic target for adult T-cell leukemia.

    Ishikawa C, Mori N

    European journal of haematology ( European Journal of Haematology )  105 ( 4 ) 460 - 467   2020.06 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • Evaluation of artesunate for the treatment of adult T-cell leukemia/lymphoma.

    Ishikawa C, Senba M, Mori N

    European journal of pharmacology ( European Journal of Pharmacology )  872   172953 - 172953   2020.04 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

    　View Summary

    Adult T-cell leukemia/lymphoma (ATLL) is an aggressive disease caused by infection with human T-cell leukemia virus type 1 (HTLV-1). Successful treatment is limited by resistance to chemotherapies. Therefore, there is an urgent need to develop novel effective strategies. Artesunate (ART), a widely used antimalarial compound, has been shown to exert cytotoxicity. Here, we aimed to assess the anti-ATLL activities of ART and to elucidate the possible molecular mechanisms involved in this effect. Compared with uninfected T cells, HTLV-1-infected T-cell lines were sensitive to ART-induced cytotoxicity. ART caused cell cycle arrest at G1 and/or G2/M phases, which was associated with decreased expression of cyclin dependent kinase 1/2/4/6, cyclin B1/D2/E and c-Myc, and increased expression of p21. ART-induced apoptosis corresponded to activation of caspase-8/9/3; decreased expression of Bcl-xL, Bcl-2, myeloid cell leukemia-1, survivin, X-linked inhibitor of apoptosis protein and cellular inhibitor of apoptosis 1/2; and increased expression of Bak. ART increased intracellular reactive oxygen species and activation of the DNA damage marker γ-H2AX. Moreover, ART-induced cytotoxicity was partly reversed by treatment with a reactive oxygen species scavenger, iron chelator, and necroptosis or ferroptosis inhibitor, suggesting the involvement of caspase-dependent and -independent lethal pathways. These effects were correlated with inhibition of nuclear factor-κB and activator protein-1 signaling through dephosphorylation of IκBα, IκB kinase (IKK) α and IKKβ, and decreased expression of JunB and JunD. Importantly, intraperitoneal injection with ART lowered tumor burden in an ATLL murine model. These preclinical results provide a rationale for evaluating the efficacy of ART in patients with ATLL.

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Other Papers 【 display / non-display 】

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