2023/10/17 更新

写真b

山本 久美子 (ヤマモト クミコ)

YAMAMOTO Kumiko

助教

職名

助教

外部リンク

出身大学院 【 表示 / 非表示

  • 北海道大学   獣医学研究科   博士課程   修了

    2016年04月 - 2020年03月

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    国名:日本国

  • 北海道教育大学   教育学研究科   教科教育専攻 理科教育専修   修士課程   修了

    2014年04月 - 2016年03月

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    国名:日本国

学位 【 表示 / 非表示

  • 博士(獣医学) ( 2020年03月   北海道大学 )

  • 修士(教育学) ( 2016年03月   北海道教育大学 )

学内職務経歴 【 表示 / 非表示

  • 東京農業大学   生物産業学部   食香粧化学科   助教

    2020年04月 - 現在

論文 【 表示 / 非表示

  • Electron Paramagnetic Resonance Implemented with Multiple Harmonic Detections Successfully Maps Extracellular pH In Vivo

    Ririko Nakaoka, Kazuhiro Kato, Kumiko Yamamoto, Hironobu Yasui, Shingo Matsumoto, Igor A. Kirilyuk, Valery V. Khramtsov, Osamu Inanami, Hiroshi Hirata

    Analytical Chemistry   2023年02月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:American Chemical Society (ACS)  

    DOI: 10.1021/acs.analchem.2c03194

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  • Metformin preferentially enhances the radio-sensitivity of cancer stem-like cells with highly mitochondrial respiration ability in HMPOS. 国際誌

    Tatsuya Deguchi, Kenji Hosoya, Shango Kim, Yusuke Murase, Kumiko Yamamoto, Tomoki Bo, Hironobu Yasui, Osamu Inanami, Mahiro Okumura

    Molecular therapy oncolytics   22   143 - 151   2021年09月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Metformin has many anti-cancer effects, alone or in combination with radiation. However, the mechanism underlying its radio-sensitized effect is still unclear, especially for cancer stem-like cells (CSCs). Here, the radio-sensitized effect of metformin was investigated, and its mechanism was revealed in CSCs derived from canine osteosarcoma cell line (HMPOS), a canine osteosarcoma cell line. Spheroid cells (SCs) were used as CSCs-rich cells derived from sphere formation, and SCs were compared with normal adherent culture cells (ACs). The radio-sensitizing effect of metformin using clonogenic assay and tumor growth in mice xenograft model were evaluated, and the mechanism of its radio-sensitization focusing on mitochondrial function was revealed. Metformin significantly enhanced radio-sensitivity of SCs through its inhibition of the mitochondrial function, as shown by decreased oxygen consumption, decreased mitochondrial membrane potential, and decreased ATP production. Additionally, SCs had a higher ability of mitochondrial respiration than ACs, which may have caused difference of their sensitivity of metformin and irradiation. In conclusion, mitochondrial function might play an important role in the sensitivity of metformin and irradiation, and drugs that target mitochondrial respiration, such as metformin, are promising radio-sensitizers to target CSCs.

    DOI: 10.1016/j.omto.2021.08.007

    PubMed

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  • Using the larvae of caddisfly as a biomonitor to assess the spatial distribution and effective half-life of radiocesium in riverine environments in Fukushima, Japan 査読あり

    Yuki Matsuo, Kunihiko Nakai, Nozomi Tatsuta, Osamu Inanami, Kumiko Yamamoto, Hazuki Mizukawa, Hiromitsu Nagasaka, Futoshi Mizutani, Youichi Chisaki, Toshiki Aiba, Takashi Ohba, Izumi Watanabe, Hiromi Nabeshi, Taiki Higuchi, Yuki Koga, Hideaki Matsumoto, Kou Nishimuta, Hideki Miyamoto, Tomokazu Haraguchi, Noriko Ryuda, Daisuke Ueno

    Physics Open   6   100060 - 100060   2021年02月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier BV  

    DOI: 10.1016/j.physo.2021.100060

  • Radiation-induced abnormal centrosome amplification and mitotic catastrophe in human cervical tumor HeLa cells and murine mammary tumor EMT6 cells 査読あり

    Masaki Fujimoto, Tomoki Bo, Kumiko Yamamoto, Hironobu Yasui, Tohru Yamamori, Osamu Inanami

    Journal of Clinical Biochemistry and Nutrition   67 ( 3 )   240 - 247   2020年11月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:The Society for Free Radical Research Japan  

    DOI: 10.3164/jcbn.19-80

  • Mitochondrial fission promotes radiation-induced increase in intracellular Ca2+ level leading to mitotic catastrophe in mouse breast cancer EMT6 cells. 査読あり

    Tomoki Bo, Tohru Yamamori, Kumiko Yamamoto, Masaki Fujimoto, Hironobu Yasui, Osamu Inanami

    Biochemical and biophysical research communications   522 ( 1 )   144 - 150   2020年01月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Mitochondrial dynamics are crucial for cellular survival in response to various stresses. Previously, we reported that Drp1 promoted mitochondrial fission after x-irradiation and its inhibition resulted in reduced cellular radiosensitivity and mitotic catastrophe. However, the mechanisms of radiation-induced mitotic catastrophe related to mitochondrial fission remain unclear. In this study, we investigated the involvement of cellular ATP production, ROS generation, and Ca2+ levels in mitotic catastrophe in EMT6 cells. Knockdown of Drp1 and Fis1, which are mitochondrial fission regulators, resulted in elongated mitochondria and significantly attenuated cellular radiosensitivity. Reduced mitochondrial fission mainly decreased mitotic catastrophe rather than necrosis and apoptosis after irradiation. Cellular ATP contents in Drp1 and Fis1 knockdown cells were similar to those in control cells. N-acetylcysteine and 2-glucopyranoside ascorbic acid have no effect on mitotic catastrophe after irradiation. The cellular [Ca2+]i level increased after irradiation, which was completely suppressed by Drp1 and Fis1 inhibition. Furthermore, BAPTA-AM significantly reduced radiation-induced mitotic catastrophe, indicating that cellular Ca2+ is a key mediator of mitotic catastrophe induction after irradiation. These results suggest that mitochondrial fission is associated with radiation-induced mitotic catastrophe via cytosolic Ca2+ regulation.

    DOI: 10.1016/j.bbrc.2019.11.027

    PubMed

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