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ID 113410
著者
叶, 奈緒美 Okayama University|Japan Society for the Promotion of Science|Tokushima University 徳島大学 教育研究者総覧
Kunisue, Narumi Okayama University
Myojin, Takumi Okayama University
Chino, Ayako Okayama University
Munemasa, Shintaro Okayama University
Murata, Yoshiyuki Okayama University
Satoh, Ayano Okayama University
Moriya, Hisao Okayama University
Nakamura, Yoshimasa Okayama University
資料タイプ
学術雑誌論文
抄録
Benzyl isothiocyanate (BITC) is a naturally-occurring isothiocyanate derived from cruciferous vegetables. BITC has been reported to inhibit the proliferation of various cancer cells, which is believed to be important for the inhibition of tumorigenesis. However, the detailed mechanisms of action remain unclear. In this study, we employed a budding yeast Saccharomyces cerevisiae as a model organism for screening. Twelve genes including MTW1 were identified as the overexpression suppressors for the antiproliferative effect of BITC using the genome-wide multi-copy plasmid collection for S. cerevisiae. Overexpression of the kinetochore protein Mtw1 counteracts the antiproliferative effect of BITC in yeast. The inhibitory effect of BITC on the proliferation of human colon cancer HCT-116 cells was consistently suppressed by the overexpression of Mis12, a human orthologue of Mtw1, and enhanced by the knockdown of Mis12. We also found that BITC increased the phosphorylated and ubiquitinated Mis12 level with consequent reduction of Mis12, suggesting that BITC degrades Mis12 through an ubiquitin-proteasome system. Furthermore, cell cycle analysis showed that the change in the Mis12 level affected the cell cycle distribution and the sensitivity to the BITC-induced apoptosis. These results provide evidence that BITC suppresses cell proliferation through the post-transcriptional regulation of the kinetochore protein Mis12.
掲載誌名
Scientific Reports
ISSN
20452322
出版者
Springer Nature
9
開始ページ
8866
発行日
2019-06-20
権利情報
© The Author(s) 2019
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言語
eng
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出版社版
部局
医学系