TY - JOUR
T1 - Inhibition of phosphatidylinositide 3-kinase ameliorates antiproliferation by benzyl isothiocyanate in human colon cancer cells
AU - Liu, Xiaoyang
AU - Takano, Chiaki
AU - Shimizu, Tomomi
AU - Yokobe, Shintaro
AU - Abe-Kanoh, Naomi
AU - Zhu, Beiwei
AU - Nakamura, Toshiyuki
AU - Munemasa, Shintaro
AU - Murata, Yoshiyuki
AU - Nakamura, Yoshimasa
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/9/9
Y1 - 2017/9/9
N2 - 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.
AB - 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.
KW - Akt
KW - Apoptosis
KW - Benzyl isothiocyanate
KW - HCT-116 cells
KW - Phosphatidylinositide 3-kinase
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U2 - 10.1016/j.bbrc.2017.07.078
DO - 10.1016/j.bbrc.2017.07.078
M3 - Article
C2 - 28712871
AN - SCOPUS:85024843941
VL - 491
SP - 209
EP - 216
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 1
ER -
