Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells
Journal Article
·
· Biochemical and Biophysical Research Communications
- Graduate School of Environmental and Life Science, Okayama University, Okayama 700-8530 (Japan)
- School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034 (China)
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.
- OSTI ID:
- 22719073
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 491; ISSN BBRCA9; ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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