加藤 優 (カトウ ユウ)

Kato, Yu

写真a

所属(所属キャンパス)

薬学部 薬学科 化学療法学講座 (芝共立)

職名

助教

メールアドレス

メールアドレス

研究室住所

東京都港区芝公園1-5-30

研究室電話番号

03-5400-2669

研究室FAX番号

03-5400-2669

学歴 【 表示 / 非表示

  • 2009年04月
    -
    2015年03月

    慶應義塾, 薬学部

    日本, 大学, 卒業

  • 2015年04月
    -
    2019年03月

    慶應義塾, 薬学部, 薬学研究科

    大学院, 修了, 博士

学位 【 表示 / 非表示

  • 博士(薬学), 慶應義塾, 課程, 2019年03月

免許・資格 【 表示 / 非表示

  • 薬剤師, 2015年05月

 

研究分野 【 表示 / 非表示

  • 医療系薬学

研究キーワード 【 表示 / 非表示

  • がん代謝

  • 上皮間葉転換

  • 分子標的薬

研究テーマ 【 表示 / 非表示

  • EMTにおけるside population細胞の誘導, 

    2019年04月
    -
    継続中

  • がん特異的な代謝ストレス応答に関する研究, 

    2015年04月
    -
    継続中

 

論文 【 表示 / 非表示

  • SNAIL- and SLUG-induced side population phenotype of HCT116 human colorectal cancer cells and its regulation by BET inhibitors

    Kato Y., Kondo S., Itakura T., Tokunaga M., Hatayama S., Katayama K., Sugimoto Y.

    Biochemical and Biophysical Research Communications (Biochemical and Biophysical Research Communications)  2019年

    研究論文(学術雑誌), 単著, 査読有り,  ISSN  0006291X

     概要を見る

    © 2019 Elsevier Inc. Epithelial-mesenchymal transition (EMT) is associated with cancer malignancies such as invasion, metastasis, and drug resistance. In this study, HCT116 human colorectal cancer cells were transduced with SLUG or SNAIL retroviruses, and EMT cells with mesenchymal morphology were established. The EMT cells showed a high invasive activity and resistance to several anticancer agents such as methotrexate, SN-38, and cisplatin. Furthermore, they contained about 1–10% side population (SP) cells that were not stained by Hoechst 33342. This SP phenotype was not stable; the isolated SP cells generated both SP and non-SP cells, suggesting a potential for differentiation. Gene expression analysis of SP cells suggested the alteration of genes that are involved in epigenetic changes. Therefore, we examined the effect of 74 epigenetic inhibitors, and found that two inhibitors, namely I-BET151 and bromosporine, targeting the bromodomain and extra-terminal motif (BET) proteins, decreased the ratio of SP cells to <50% compared with the control, without affecting the immediate efflux of Hoechst 33342 by transporters. In addition, compared with the parental cells, the EMT cells showed a higher sensitivity to I-BET151 and bromosporine. This study suggests that EMT development and SP phenotype can be independent events but both are regulated by BET inhibitors in SLUG- or SNAIL-transducted HCT116 cells.

  • BCR-ABL tyrosine kinase inhibition induces metabolic vulnerability by preventing the integrated stress response in K562 cells

    Kato Y., Kunimasa K., Sugimoto Y., Tomida A.

    Biochemical and Biophysical Research Communications (Biochemical and Biophysical Research Communications)  504 ( 4 ) 721 - 726 2018年10月

    ISSN  0006291X

     概要を見る

    © 2018 Elsevier Inc. The integrated stress response (ISR) is a cellular process that is characterized by activation of eukaryotic initiation factor (eIF)2α kinases and subsequent induction of activating transcription factor (ATF)4. The ISR plays an important role in protecting cells from tumor-related metabolic stresses, such as nutrient deprivation and perturbed proteostasis. Here, we showed that disruption of the ISR, together with increased cellular stress vulnerability, was produced by pharmacological inhibition of BCR-ABL, the oncogenic driver in chronic myeloid leukemia (CML). Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2α kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress. Prevention of ATF4 induction likely occurred as a result of the combinatorial suppression of the eIF2α kinase and phosphoinositide 3-kinase/mammalian target of rapamycin signaling pathways. In addition, we found that pharmacological inhibition of PERK mimicked BCR-ABL inhibition to enhance apoptosis induction under stress conditions. These findings indicate that the ISR is under the control of BCR-ABL and may foster adaptation to tumorigenic stresses in CML cells.

研究発表 【 表示 / 非表示

  • ABCB5発現細胞におけるGLS発現の増大

    第78回 日本癌学会学術集会, 2019年09月, ポスター(一般)

  • 上皮間葉転換に伴って誘導されるside population細胞の制御

    第78回 日本癌学会学術集会, 2019年09月, ポスター(一般)

  • FLT3-ITDによるIntegrated Stress Responseの制御

    第63回 日本薬学会 関東支部大会, 2019年09月, ポスター(一般)

  • P-glycoproteinの発現を制御するタンパク質の探索

    第63回 日本薬学会 関東支部大会, 2019年09月, ポスター(一般)

  • JQ1耐性細胞の解析

    第63回 日本薬学会関東支部大会, 2019年09月, ポスター(一般)

全件表示 >>

 

担当授業科目 【 表示 / 非表示

  • 課題研究(化学療法学)

    2019年度

  • 演習(化学療法学)

    2019年度

  • 卒業研究A

    2019年度

  • 薬学英語演習K

    2019年度

  • 微生物学実習

    2019年度

全件表示 >>