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ID 57790
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Abe-Kanoh, Naomi Graduate School of Environmental and Life Science, Okayama University
Kunisue, Narumi Graduate School of Environmental and Life Science, Okayama University
Myojin, Takumi Graduate School of Environmental and Life Science, Okayama University
Chino, Ayako Research Core for Interdisciplinary Sciences, Okayama University
Munemasa, Shintaro Graduate School of Environmental and Life Science, Okayama University
Murata, Yoshiyuki Graduate School of Environmental and Life Science, Okayama University ORCID Kaken ID publons researchmap
Satoh, Ayano Graduate School of Natural Science and Technology, Okayama University ORCID Kaken ID publons researchmap
Moriya, Hisao Research Core for Interdisciplinary Sciences, Okayama University ORCID Kaken ID publons researchmap
Nakamura, Yoshimasa Graduate School of Environmental and Life Science, Okayama University, Okayama ORCID Kaken ID publons researchmap
Abstract
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.
Published Date
2019-6-20
Publication Title
Scientific Reports
Volume
volume9
Publisher
Nature Publishing Group
Start Page
8866
ISSN
2045-2322
Content Type
Journal Article
language
英語
OAI-PMH Set
岡山大学
Copyright Holders
© The Author(s) 2019
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DOI
Web of Science KeyUT
Related Url
isVersionOf https://doi.org/10.1038/s41598-019-45248-2
License
https://creativecommons.org/licenses/by/4.0/
Funder Name
Japan Society for the Promotion of Science
助成番号
25292073