KONDO Shingo



Faculty of Pharmacy, Department of Pharmacy Chemotherapy (Shiba-Kyoritsu)


Research Associate/Assistant Professor/Instructor

E-mail Address

E-mail address

Contact Address

1-5-30 shibakoen, Minato-ku, Tokyo

Telephone No.


Fax No.


Career 【 Display / hide

  • 2017.04

    Medical Hospital, Tokyo Medical and Dental University, Department of Pharmacy, pharmacist

Academic Background 【 Display / hide

  • 2013.04

    Keio University

    Graduate School, Completed, Doctoral course

Academic Degrees 【 Display / hide

  • Doctor(Pharmacy), Keio University, Coursework, 2017.03

Licenses and Qualifications 【 Display / hide

  • Pharmacist license, 2013.07


Papers 【 Display / hide

  • Effect of TNIK upregulation on JQ1-resistant human colorectal cancer HCT116 cells

    Takahashi C., Kondo S., Sadaoka K., Ishizuka S., Noguchi K., Kato Y., Sugimoto Y.

    Biochemical and Biophysical Research Communications (Biochemical and Biophysical Research Communications)  530 ( 1 ) 230 - 234 2020.06

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  0006291X

     View Summary

    © 2020 Elsevier Inc. JQ1 disrupts the binding of bromodomain and extra-terminal (BET) family of proteins to acetylated histones, modulates the expression of various genes, and inhibits the proliferation of cancer cells. We established two JQ1-resistant sublines from human colorectal cancer HCT116 cells. These resistant cells showed an 8- to 9-fold higher resistance to JQ1, and a 2- to 4-fold higher resistance to various anti-cancer agents, such as doxorubicin, etoposide, mitoxantrone, SN-38, cisplatin, and methotrexate than the parental HCT116 cells. The JQ1-resistant cells expressed higher levels of TRAF2 and NCK-interacting protein kinase (TNIK), cyclin D1 (CCND1), cyclin E1 (CCNE1), and their corresponding mRNAs than the parental cells. TNIK is a regulator of Wnt/β-catenin signaling and is known to transactivate CCND1. Transient transfection of HCT116 cells with a TNIK expression plasmid resulted in the upregulation of cyclin D1, cyclin E1, and their corresponding mRNAs, as well as an increase in CCNE1 promoter activity. Furthermore, luciferase assay revealed that the JQ1-resistant cells showed high CCNE1 promoter activity. These results suggest that TNIK also transactivates CCNE1. Three stable TNIK transfectant clones of HEK293 cells expressed 1.5- to 2-fold higher levels of TNIK, cyclin D1, and cyclin E1 than the parental cells. The 293/TNIK-6 cells, which expressed the highest level of TNIK among the transfectants, showed a 2.3-fold higher resistance to JQ1 than the parental cells. These results suggest the possible involvement of TNIK in cellular resistance to JQ1.

  • STAT1 upregulates glutaminase and modulates amino acids and glutathione metabolism

    Kondo S., Kato Y., Minagawa S., Sugimoto Y.

    Biochemical and Biophysical Research Communications (Biochemical and Biophysical Research Communications)  523 ( 3 ) 672 - 677 2020.01

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  0006291X

     View Summary

    © 2020 Elsevier Inc. We previously reported the upregulation of cellular Glu and glutathione levels in human ABCB5- and murine Abcb5-transfected cells. Here, we demonstrate the upregulation of STAT1 and glutaminase (GLS) in ABCB5/Abcb5-transfected cells. Among a total of four ABCB5/Abcb5 high-expressing clones with docetaxel resistance, three of the clones expressed STAT1 and GLS highly and showed resistance to docetaxel and buthionine sulfoximine (BSO), an inhibitor of glutathione synthesis. Neither STAT1 nor GLS upregulation was observed in the remaining ABCB5 high-expressing clone, as well as in another two ABCB5 low-expressing clones; these three clones did not show BSO resistance. The ABCB5/STAT1 high-expressing clones showed higher cellular levels of Ala, Glu, and Asp and lower cellular levels of Phe, Trp, Leu, Ile, Gly, Met, Tyr, Val, and His compared to the ABCB5/STAT1 low-expressing clones. The former clones also showed a higher resistance to Glu. The STAT1-transfected clones expressed high levels of GLS and the corresponding mRNA, suggesting the transactivation of GLS by STAT1. These clones showed resistance to Glu and BSO, similar to the ABCB5/STAT1 high-expressing clones. The cellular glutathione levels of the STAT1-transfected clones were significantly higher than that of the control. The STAT1-transfected clones also showed greater resistance to the effect of BSO on the cellular glutathione depletion compared to the control. These results demonstrate that STAT1 upregulates GLS and modulates amino acids and glutathione metabolism. Although we were unable to directly prove STAT1 upregulation by ABCB5, our results suggest that ABCB5 expression, directly or indirectly, leads to the overexpression of STAT1.

  • 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.

    Biochem Biophys Res Commun. (Biochemical and Biophysical Research Communications)  521 ( 1 ) 152 - 157 2019.10

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  0006291X

     View Summary

    © 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.

  • Upregulation of cellular glutathione levels in human ABCB5- and murine Abcb5-transfected cells.

    Kondo S., Hongama K., Hanaya K., Yoshida R., Kawanobe T., Katayama K., Noguchi K., Sugimoto Y.

    BMC Pharmacol Toxicol.  2015.12

    Research paper (scientific journal), Joint Work, Accepted

Papers, etc., Registered in KOARA 【 Display / hide

Reviews, Commentaries, etc. 【 Display / hide

  • ヒスチジン異化はメトトレキサート感受性の主要な決定因子である

    近藤 慎吾

    ファルマシア (公益社団法人日本薬学会 )  55 ( 7 ) 702 2019.07

    Book review and document introduction, etc., Single Work

Presentations 【 Display / hide

  • xCT upregulation and ferroptosis resistance in SLUG-transfected HCT116 cells

    加藤 優, 近藤 慎吾, 杉本 芳一

    第24回日本がん分子標的治療学会学術集会 (徳島グランヴィリオホテル) , 2020.10, Poster (general)

  • STAT1-mediated drug resistance and its circumvention

    近藤 慎吾, 加藤 優, 杉本 芳一

    第79回日本癌学会学術総会, 2020.10, Poster (general)

  • Factors affecting the ferroptosis sensitivity of SLUG-transduced HCT116 cells

    加藤 優, 近藤 慎吾, 杉本 芳一

    第79回日本癌学会学術総会 (広島) , 2020.10, Poster (general)

  • Upregulation of the GLS expression in the ABCB5-expressing cells

    近藤 慎吾, 加藤 優, 杉本 芳一

    第78回日本癌学会学術総会 (京都国際会館) , 2019.09, Poster (general)

  • Regulation of side population cells induced by epithelial-mesenchymal transition

    加藤 優, 近藤 慎吾, 片山 和浩, 杉本 芳一

    第78回日本癌学会学術総会 (京都国際会館) , 2019.09, Poster (general)

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Courses Taught 【 Display / hide











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Memberships in Academic Societies 【 Display / hide

  • 日本がん分子標的治療学会, 

  • 日本癌学会, 

  • 日本薬学会,