Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells

Xiaoyang Liu; Naomi Abe-Kanoh; Yujia Liu; Beiwei Zhu; Shintaro Munemasa; Toshiyuki Nakamura; Yoshiyuki Murata; Yoshimasa Nakamura

doi:10.1080/09168451.2017.1374830

Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells

Xiaoyang Liu, Naomi Abe-Kanoh, Yujia Liu, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

The regulating role of phosphatidylinositide 3-ki-nase (PI3K) in benzyl isothiocyanate (BITC)-induced Nrf2 activation, contributing to the inducible expression of cytoprotective genes, was investigated. BITC significantly enhanced the accumulation of Nrf2 as well as autophagic molecules in human colorectal cancer HCT-116 cells. Experiments using a PI3K-specific inhibitor suggested that PI3K plays the key role in the non-canonical Nrf2 activation by BITC.

Original language	English
Pages (from-to)	2212-2215
Number of pages	4
Journal	Bioscience, Biotechnology and Biochemistry
Volume	81
Issue number	11
DOIs	https://doi.org/10.1080/09168451.2017.1374830
Publication status	Published - 2017

Keywords

Autophagy
Benzyl isothiocyanate
Keap1
Nrf2
Phosphatidylinositide 3-kinase

ASJC Scopus subject areas

Biotechnology
Analytical Chemistry
Biochemistry
Applied Microbiology and Biotechnology
Molecular Biology
Organic Chemistry

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/09168451.2017.1374830

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Liu, X., Abe-Kanoh, N., Liu, Y., Zhu, B., Munemasa, S., Nakamura, T., Murata, Y., & Nakamura, Y. (2017). Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells. Bioscience, Biotechnology and Biochemistry, 81(11), 2212-2215. https://doi.org/10.1080/09168451.2017.1374830

Liu, X, Abe-Kanoh, N, Liu, Y, Zhu, B, Munemasa, S , Nakamura, T , Murata, Y & Nakamura, Y 2017, 'Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells', Bioscience, Biotechnology and Biochemistry, vol. 81, no. 11, pp. 2212-2215. https://doi.org/10.1080/09168451.2017.1374830

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title = "Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells",

abstract = "The regulating role of phosphatidylinositide 3-ki-nase (PI3K) in benzyl isothiocyanate (BITC)-induced Nrf2 activation, contributing to the inducible expression of cytoprotective genes, was investigated. BITC significantly enhanced the accumulation of Nrf2 as well as autophagic molecules in human colorectal cancer HCT-116 cells. Experiments using a PI3K-specific inhibitor suggested that PI3K plays the key role in the non-canonical Nrf2 activation by BITC.",

keywords = "Autophagy, Benzyl isothiocyanate, Keap1, Nrf2, Phosphatidylinositide 3-kinase",

author = "Xiaoyang Liu and Naomi Abe-Kanoh and Yujia Liu and Beiwei Zhu and Shintaro Munemasa and Toshiyuki Nakamura and Yoshiyuki Murata and Yoshimasa Nakamura",

note = "Funding Information: *Corresponding author. Email: yossan@cc.okayama-u.ac.jp ‡A recipient of a doctoral scholarship from the China Scholarship Council. Funding Information: This study was partly supported by MEXT KAKENHI [grant number 25292073], [grant number16K14928], [grant number17H03818] (YN). Publisher Copyright: {\textcopyright} 2017 Japan Society for Bioscience, Biotechnology, and Agrochemistry.",

year = "2017",

doi = "10.1080/09168451.2017.1374830",

language = "English",

volume = "81",

pages = "2212--2215",

journal = "Bioscience, Biotechnology and Biochemistry",

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T1 - Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells

AU - Liu, Xiaoyang

AU - Abe-Kanoh, Naomi

AU - Liu, Yujia

AU - Zhu, Beiwei

AU - Munemasa, Shintaro

AU - Nakamura, Toshiyuki

AU - Murata, Yoshiyuki

AU - Nakamura, Yoshimasa

N1 - Funding Information: *Corresponding author. Email: yossan@cc.okayama-u.ac.jp ‡A recipient of a doctoral scholarship from the China Scholarship Council. Funding Information: This study was partly supported by MEXT KAKENHI [grant number 25292073], [grant number16K14928], [grant number17H03818] (YN). Publisher Copyright: © 2017 Japan Society for Bioscience, Biotechnology, and Agrochemistry.

PY - 2017

Y1 - 2017

N2 - The regulating role of phosphatidylinositide 3-ki-nase (PI3K) in benzyl isothiocyanate (BITC)-induced Nrf2 activation, contributing to the inducible expression of cytoprotective genes, was investigated. BITC significantly enhanced the accumulation of Nrf2 as well as autophagic molecules in human colorectal cancer HCT-116 cells. Experiments using a PI3K-specific inhibitor suggested that PI3K plays the key role in the non-canonical Nrf2 activation by BITC.

AB - The regulating role of phosphatidylinositide 3-ki-nase (PI3K) in benzyl isothiocyanate (BITC)-induced Nrf2 activation, contributing to the inducible expression of cytoprotective genes, was investigated. BITC significantly enhanced the accumulation of Nrf2 as well as autophagic molecules in human colorectal cancer HCT-116 cells. Experiments using a PI3K-specific inhibitor suggested that PI3K plays the key role in the non-canonical Nrf2 activation by BITC.

KW - Autophagy

KW - Benzyl isothiocyanate

KW - Keap1

KW - Nrf2

KW - Phosphatidylinositide 3-kinase

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JO - Bioscience, Biotechnology and Biochemistry

JF - Bioscience, Biotechnology and Biochemistry

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ER -

Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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