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

被引：9
|
作者：
Liu, Xiaoyang [1 ,2 ]
Abe-Kanoh, Naomi [1 ,3 ]
Liu, Yujia [1 ,2 ]
Zhu, Beiwei [2 ]
Munemasa, Shintaro [1 ]
Nakamura, Toshiyuki [1 ]
Murata, Yoshiyuki [1 ]
Nakamura, Yoshimasa [1 ]
机构：
[1] Okayama Univ, Grad Sch Environm & Life Sci, Okayama, Japan
[2] Dalian Polytech Univ, Sch Food Sci & Technol, Dalian, Peoples R China
[3] Tokushima Univ, Inst Biomed Sci, Dept Food Sci, Grad Sch, Tokushima, Japan
来源：
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY | 2017年 / 81卷 / 11期
关键词：
autophagy; phosphatidylinositide; 3-kinase; Nrf2; Keap1; benzyl isothiocyanate; PATHWAY; RESISTANCE;
D O I：
10.1080/09168451.2017.1374830
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The regulating role of phosphatidylinositide 3-kinase (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.
引用
收藏
页码：2212 / 2215
页数：4
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