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

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. - Highlights: • Benzyl isothiocyanate (BITC) activates PI3K/Akt/FoxO survival pathway. • PI3K inhibitors significantly enhance the BITC-induced antiproliferation. • The MEK/ERK pathway is ruled out in the mechanism of BITC resistance. • BITC enhances the insulin-activated PI3K/Akt/FoxO pathway by PTP1B inhibition. • The PI3K/Akt/FoxO pathway negatively regulates the BITC-induced antiproliferation.

Authors:
 [1];  [2]; ; ;  [1];  [1];  [3];  [4]; ; ;  [1];  [1]
  1. Graduate School of Environmental and Life Science, Okayama University, Okayama 700-8530 (Japan)
  2. (China)
  3. (Japan)
  4. School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034 (China)
Publication Date:
OSTI Identifier:
22719073
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 491; Journal Issue: 1; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; ATTENUATION; INHIBITION; INSULIN; IODIDES; ISOTHIOCYANATES; LARGE INTESTINE; MITOGENS; NEOPLASMS; PHOSPHATASES; PHOSPHOTRANSFERASES; RECEPTORS; TYROSINE

Citation Formats

Liu, Xiaoyang, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, Takano, Chiaki, Shimizu, Tomomi, Yokobe, Shintaro, Abe-Kanoh, Naomi, Department of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8503, Zhu, Beiwei, Nakamura, Toshiyuki, Munemasa, Shintaro, Murata, Yoshiyuki, and Nakamura, Yoshimasa. Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells. United States: N. p., 2017. Web. doi:10.1016/J.BBRC.2017.07.078.
Liu, Xiaoyang, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, Takano, Chiaki, Shimizu, Tomomi, Yokobe, Shintaro, Abe-Kanoh, Naomi, Department of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8503, Zhu, Beiwei, Nakamura, Toshiyuki, Munemasa, Shintaro, Murata, Yoshiyuki, & Nakamura, Yoshimasa. Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells. United States. doi:10.1016/J.BBRC.2017.07.078.
Liu, Xiaoyang, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, Takano, Chiaki, Shimizu, Tomomi, Yokobe, Shintaro, Abe-Kanoh, Naomi, Department of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8503, Zhu, Beiwei, Nakamura, Toshiyuki, Munemasa, Shintaro, Murata, Yoshiyuki, and Nakamura, Yoshimasa. Sat . "Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells". United States. doi:10.1016/J.BBRC.2017.07.078.
@article{osti_22719073,
title = {Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells},
author = {Liu, Xiaoyang and School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034 and Takano, Chiaki and Shimizu, Tomomi and Yokobe, Shintaro and Abe-Kanoh, Naomi and Department of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8503 and Zhu, Beiwei and Nakamura, Toshiyuki and Munemasa, Shintaro and Murata, Yoshiyuki and Nakamura, Yoshimasa},
abstractNote = {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. - Highlights: • Benzyl isothiocyanate (BITC) activates PI3K/Akt/FoxO survival pathway. • PI3K inhibitors significantly enhance the BITC-induced antiproliferation. • The MEK/ERK pathway is ruled out in the mechanism of BITC resistance. • BITC enhances the insulin-activated PI3K/Akt/FoxO pathway by PTP1B inhibition. • The PI3K/Akt/FoxO pathway negatively regulates the BITC-induced antiproliferation.},
doi = {10.1016/J.BBRC.2017.07.078},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 491,
place = {United States},
year = {2017},
month = {9}
}