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

作者：Xiaoyang Liu, Naomi Abe‐Kanoh, Yujia Liu, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura · 发表于：Bioscience Biotechnology and Biochemistry · 年份：2017 · DOI：10.1080/09168451.2017.1374830 · 被引用次数：17 · 研究领域：Genomics, phytochemicals, and oxidative stress、Autophagy in Disease and Therapy、Glutathione Transferases and Polymorphisms

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.