Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells
Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells
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DOI：
10.1080/09168451.2017.1374830
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发表时间：
2017-09
期刊：
影响因子：
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通讯作者：
Xiaoyang Liu;Naomi Abe-Kanoh;Yujia Liu;B. Zhu;S. Munemasa;Toshiyuki Nakamura;Y. Murata;Yoshimasa Nakamura
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文献类型：
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作者：
Xiaoyang Liu;Naomi Abe-Kanoh;Yujia Liu;B. Zhu;S. Munemasa;Toshiyuki Nakamura;Y. Murata;Yoshimasa Nakamura
研究了PI3K在异硫氰酸苄酯（BITC）诱导的Nrf2激活中的调节作用，并对细胞保护基因的诱导表达起作用。BITC显著增强了人结直肠癌HCT-116细胞中Nrf2和自噬分子的积累。使用PI3K特异性抑制剂的实验表明，PI3K在BITC激活非典型Nrf2中起关键作用。
The regulating role of phosphatidylinositide 3-kinase (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.