A millet bran-derived peroxidase inhibits cell migration by antagonizing STAT3-mediated epithelial-mesenchymal transition in human colon cancer

被引:16
作者
Shan, Shuhua [1 ,2 ]
Li, Zongwei [1 ]
Guo, Songjia [1 ,3 ]
Li, Zhuoyu [1 ,4 ]
Shi, Tonglin [1 ]
Shi, Jiangying [1 ]
机构
[1] Shanxi Univ, Inst Biotechnol, Key Lab Chem Biol & Mol Engn, Natl Minist Educ, Taiyuan 030006, Peoples R China
[2] Taiyuan Normal Univ, Dept Biol, Taiyuan 030031, Peoples R China
[3] Shanxi Med Univ, Fenyang Coll, Dept Lab Med, Fenyang 032200, Shanxi, Peoples R China
[4] Zhejiang Chinese Med Univ, Coll Life Sci, Hangzhou 310053, Zhejiang, Peoples R China
基金
山西省青年科学基金; 中国国家自然科学基金;
关键词
Foxtail millet bran; FMBP; Colon cancer; Cell migration; Epithelial-mesenchymal transition; STAT3; ADHESION MOLECULES; STAT3; ACTIVATION; INVASION; GROWTH; ANTIOXIDANT; PROMOTION; APOPTOSIS; PHENOLICS; FAMILY; TWIST;
D O I
10.1016/j.jff.2014.07.005
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Foxtail millet (Setaria italica) is one of the most important food crops in Northern China. The millet-derived antioxidant components play important roles in disease prevention. Here, we reported a peroxidase from foxtail millet bran, named FMBP, could display anti-migration effects on human colon cancer cells of DLD1. Notably, it had no effects on the normal colon epithelial cells of FHC. The anti-migration effects of FMBP were mainly realized by virtue of antagonizing epithelial-mesenchymal transition (EMT). Mechanistically, PMBP treatment decreased the phosphorylation of JAK1 and its downstream signaling molecular STAT3, followed by the reduced expression of c-Myc and Snail1, both of them are critical regulators of EMT. Consistently, STAT3 overexpression could partially reverse the migration inhibition caused by FMBP. It demonstrated that PMBP hampered colon cancer cell migration by targeting the STAT3 pathway. Therefore, the millet bran-derived peroxidase may be exploited as a natural therapeutic agent against colon cancer metastasis. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:444 / 455
页数:12
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