附属病院 臨床研究センター 臨床研究・治験推進部

和田 妙子

ワダ タエコ  (Taeko Wada)

基本情報

所属
自治医科大学 附属病院臨床研究センター臨床研究・治験推進部 学内准教授
学位
医学博士(自治医科大学)

通称等の別名
和田 妙子
研究者番号
30382956
ORCID ID
 https://orcid.org/0000-0001-6825-8559
J-GLOBAL ID
201401083241584853
researchmap会員ID
B000237836

外部リンク

論文

 26
  • Kenji Tago, Satoshi Ohta, Chihiro Aoki-Ohmura, Megumi Funakoshi-Tago, Miho Sashikawa, Takeshi Matsui, Yuki Miyamoto, Taeko Wada, Tomoyuki Oshio, Mayumi Komine, Jitsuhiro Matsugi, Yusuke Furukawa, Mamitaro Ohtsuki, Junji Yamauchi, Ken Yanagisawa
    Scientific reports 11(1) 20658-20658 2021年10月19日  
    NKIRAS1 and NKIRAS2 (also called as κB-Ras) were identified as members of the atypical RAS family that suppress the transcription factor NF-κB. However, their function in carcinogenesis is still controversial. To clarify how NKIRAS acts on cellular transformation, we generated transgenic mice in which NKIRAS2 was forcibly expressed using a cytokeratin 15 (K15) promoter, which is mainly activated in follicle bulge cells. The ectopic expression of NKIRAS2 was mainly detected in follicle bulges of transgenic mice with NKIRAS2 but not in wild type mice. K15 promoter-driven expression of NKIRAS2 failed to affect the development of epidermis, which was evaluated using the expression of K10, K14, K15 and filaggrin. However, K15 promoter-driven expression of NKIRAS2 effectively suppressed the development of skin tumors induced by treatment with 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol 13-acetate (TPA). This observation suggested that NKIRAS seemed to function as a tumor suppressor in follicle bulges. However, in the case of oncogenic HRAS-driven cellular transformation of murine fibroblasts, knockdown of NKIRAS2 expression drastically suppressed HRAS-mutant-provoked cellular transformation, suggesting that NKIRAS2 was required for the cellular transformation of murine fibroblasts. Furthermore, moderate enforced expression of NKIRAS2 augmented oncogenic HRAS-provoked cellular transformation, whereas an excess NKIRAS2 expression converted its functional role into a tumor suppressive phenotype, suggesting that NKIRAS seemed to exhibit a biphasic bell-shaped enhancing effect on HRAS-mutant-provoked oncogenic activity. Taken together, the functional role of NKIRAS in carcinogenesis is most likely determined by not only cellular context but also its expression level.
  • Junya Tamaoki, Miki Takeuchi, Ryo Abe, Hiroshi Kaneko, Taeko Wada, Shinjiro Hino, Mitsuyoshi Nakao, Yusuke Furukawa, Makoto Kobayashi
    Scientific reports 10(1) 8521-8521 2020年5月22日  査読有り
    LSD1/KDM1A is a widely conserved lysine-specific demethylase that removes methyl groups from methylated proteins, mainly histone H3. We previously isolated the zebrafish LSD1 gene and demonstrated that it is required for primitive hematopoiesis. Recently, a neuron-specific splicing variant of LSD1 was found in mammals and its specific functions and substrate specificities were reported. To our surprise, zebrafish LSD1 cDNA, which we previously analyzed, was corresponded to the neuron-specific variant in mammals. In this study, we investigated the structures and expression of LSD1 splicing variants in zebrafish and found all 4 types of LSD1 isoforms: LSD1, LSD1+2al, LSD1+8al and LSD1+2al8al. Interestingly, LSD1+8al/LSD1+2al8al, which correspond to mammalian neuron-specific variants, expressed ubiquitously in zebrafish. We also performed phenotypic rescue experiments of a zebrafish LSD1 mutant (kdm1ait627) using human and zebrafish LSD1 variants to identify which variant is involved in primitive hematopoiesis. Unexpectedly, the overexpression of all types of human and zebrafish variants was able to rescue the hematopoietic phenotypes in LSD1 mutants. Furthermore, enzymatic-deficient LSD1K661A (human) and K638A (zebrafish) were also able to rescue the mutant phenotypes. These results suggest that the LSD1 functions in zebrafish primitive hematopoiesis are free from any splicing-dependent regulation or demethylation reaction.
  • Taeko Wada, Jiro Kikuchi, Daisuke Koyama, Hiroaki Honda, Yusuke Furukawa
    Leukemia research 82 29-32 2019年7月  査読有り
  • 古川 雄祐, 和田 妙子, 菊池 次郎
    血液内科 72(6) 857-862 2016年6月  
  • 和田 妙子, 小山 大輔, 菊池 次郎, 本田 浩章, 古川 雄祐
    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 88回・38回 [3T18-04(3P1036)] 2015年12月  

MISC

 28

講演・口頭発表等

 3

共同研究・競争的資金等の研究課題

 4