研究者業績

稲熊 容子

イナグマ ヨウコ  (yoko inaguma)

基本情報

所属
藤田医科大学 医学部 教養

J-GLOBAL ID
201501012704629618
researchmap会員ID
7000012782

論文

 22
  • Akihiro Abe, Yukiya Yamamoto, Akira Katsumi, Hideyuki Yamamoto, Akinao Okamoto, Yoko Inaguma, Chisako Iriyama, Masutaka Tokuda, Masataka Okamoto, Nobuhiko Emi, Akihiro Tomita
    Cytogenetic and genome research 2020年6月16日  査読有り
    Fusions of the Runt-related transcription factor 1 (RUNX1) with different partner genes have been associated with various hematological disorders. Interestingly, the C-terminally truncated form of RUNX1 and RUNX1 fusion proteins are similarly considered important contributors to leukemogenesis. Here, we describe a 59-year-old male patient who was initially diagnosed with acute myeloid leukemia, inv(16)(p13;q22)/CBFB-MYH11 (FAB classification M4Eo). He achieved complete remission and negative CBFB-MYH11 status with daunorubicin/cytarabine combination chemotherapy but relapsed 3 years later. Cytogenetic analysis of relapsed leukemia cells revealed CBFB-MYH11 negativity and complex chromosomal abnormalities without inv(16)(p13;q22). RNA-seq identified the glutamate receptor, ionotropic, kinase 2 (GRIK2) gene on 6q16 as a novel fusion partner for RUNX1 in this case. Specifically, the fusion of RUNX1 to the GRIK2 antisense strand (RUNX1-GRIK2as) generated multiple missplicing transcripts. Because extremely low levels of wild-type GRIK2 were detected in leukemia cells, RUNX1-GRIK2as was thought to drive the pathogenesis associated with the RUNX1-GRIK2 fusion. The truncated RUNX1 generated from RUNX1-GRIK2as induced the expression of the granulocyte colony-stimulating factor (G-CSF) receptor on 32D myeloid leukemia cells and enhanced proliferation in response to G-CSF. In summary, the RUNX1-GRIK2as fusion emphasizes the importance of aberrantly truncated RUNX1 in leukemogenesis.
  • Abe A, Yamamoto Y, Katsumi A, Okamoto A, Tokuda M, Inaguma Y, Yamamoto K, Yanada M, Kanie T, Tomita A, Akatsuka Y, Okamoto M, Kameyama T, Mayeda A, Emi N
    International Journal of Hematology 108(2) 208-212 2018年8月  査読有り
  • Akinao Okamoto, Masamitsu Yanada, Yoko Inaguma, Masutaka Tokuda, Satoko Morishima, Tadaharu Kanie, Yukiya Yamamoto, Shuichi Mizuta, Yoshiki Akatsuka, Tetsushi Yoshikawa, Yoshikazu Mizoguchi, Shigeo Nakamura, Masataka Okamoto, Nobuhiko Emi
    Hematological Oncology 35(1) 87-93 2017年3月1日  査読有り
  • C. Balachandran, N. Emi, Y. Arun, N. Yamamoto, V. Duraipandiyan, Yoko Inaguma, Akinao Okamoto, S. Ignacimuthu, N. A. Al-Dhabi, P. T. Perumal
    CHEMICO-BIOLOGICAL INTERACTIONS 249 23-35 2016年4月  査読有り
    The present study investigated the anticancer activity of 2,3-dihydroxy-9,10-anthraquinone against different cancer cells such as MCF-7, COLO320, HepG-2, Skov-3, MOLM-14, NB-4, CEM, K562, Jurkat, HL-60, U937, IM-9 and Vero. 2,3-dihydroxy-9,10-anthraquinone showed good antiproliferative activity against COLO320 cells when compared to other tested cells. The cytotoxicity results showed 79.8% activity at the dose of 2.07 mu M with IC50 value of 0.13 mu M at 24 h in COLO320 cells. So we chose COLO320 cells for further anticancer studies. mRNA expression was confirmed by qPCR analysis using SYBR green method. Treatment with 2,3-dihydroxy-9,10-anthraquinone was found to trigger intrinsic apoptotic pathway as indicated by down regulation of Bcl-2, Bcl-xl; up regulation of Bim, Bax, Bad; release of cytochrome c and pro-caspases cleaving to caspases. Furthermore, 2,3-dihydroxy-9,10-anthraquinone stopped at G0/G1 phase with modulation in protein levels of cyclins. On the other hand PI3K/AKT signaling plays an important role in cell metabolism. We found that 2,3-dihydroxy-9,10-anthraquinone inhibits PI3K/AKT activity after treatment. Also, COX-2 enzyme plays a major role in colorectal cancer. Our results showed that the treatment significantly reduced COX-2 enzyme in COLO320 cells. These results indicated antiproliferative activity of 2,3-dihydroxy-9,10-anthraquinone involving apoptotic pathways, mitochondrial functions, cell cycle checkpoint and controlling the over expression genes during the colorectal cancer. Molecular docking studies showed that the compound bound stably to the active sites of Bcl-2, COX-2, PI3K and AKT. This is the first report of anticancer mechanism involving 2,3-dihydroxy-9,10-anthraquinone in COLO320 cells. The present results might provide helpful suggestions for the design of antitumor drugs toward colorectal cancer treatment. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

MISC

 53

書籍等出版物

 4

講演・口頭発表等

 11