Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells

Xiaoyang Liu, Chiaki Takano, Tomomi Shimizu, Shintaro Yokobe, Naomi Abe-Kanoh, Beiwei Zhu, Toshiyuki Nakamura, Shintaro Munemasa, Yoshiyuki Murata, Yoshimasa Nakamura

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

In the present study, we clarified the role of phosphatidylinositide 3-kinase (PI3K) in antiproliferation induced by benzyl isothiocyanate (BITC) in human colorectal cancer cells. BITC simultaneously activated the PI3K/Akt/forkhead box O (FoxO) pathway, whereas it significantly inhibited the proliferation in human colorectal cancer cells. Inhibitory experiments using a PI3K selective inhibitor, LY294002 or NVP-BEZ235, significantly enhanced the BITC-induced antiproliferation and apoptotic cell population with the attenuation of the BITC-induced activation of the PI3K/Akt/FoxO survival pathway. Furthermore, BITC enhanced the insulin-activated PI3K/Akt/FoxO pathway, possibly through its inhibition of the protein tyrosine phosphatase 1B enzymatic activity. Taken together, these results suggested that the PI3K/Akt/FoxO pathway negatively regulates the BITC-induced antiproliferation in human colorectal cancer cells.

Original languageEnglish
Pages (from-to)209-216
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume491
Issue number1
DOIs
Publication statusPublished - Sep 9 2017

Keywords

  • Akt
  • Apoptosis
  • Benzyl isothiocyanate
  • HCT-116 cells
  • Phosphatidylinositide 3-kinase

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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