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

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2 Citations (Scopus)


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 languageEnglish
Pages (from-to)2212-2215
Number of pages4
JournalBioscience, Biotechnology and Biochemistry
Issue number11
Publication statusPublished - Jan 1 2017



  • Autophagy
  • Benzyl isothiocyanate
  • Keap1
  • Nrf2
  • Phosphatidylinositide 3-kinase

ASJC Scopus subject areas

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

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