MYC associated zinc finger protein promotes the invasion and metastasis of hepatocellular carcinoma by inducing epithelial mesenchymal transition

被引:39
|
作者
Luo, Wei [1 ]
Zhu, Xiaonian [1 ]
Liu, Wei [1 ]
Ren, Yuan [1 ]
Bei, Chunhua [1 ]
Qin, Linyuan [1 ]
Miao, Xueyan [1 ]
Tang, Fen [2 ]
Tang, Guifang [2 ]
Tan, Shengkui [1 ]
机构
[1] Guilin Med Univ, Sch Publ Hlth, Guilin 541004, Guangxi, Peoples R China
[2] Guilin Med Univ, Affiliated Nanxishan Hosp, Dept Hepatol, Guilin 541004, Guangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
MYC associated zinc finger protein (MAZ); hepatocellular carcinoma (HCC); zinc finger E-box binding homeobox 1 (ZEB1); zinc finger E-box binding homeobox 2 (ZEB2); epithelial-mesenchymal transition (EMT); E-CADHERIN; CANCER STATISTICS; TUMOR; MAZ; EXPRESSION; CELLS; ZEB2; ANGIOGENESIS; PERMEABILITY; INDUCTION;
D O I
10.18632/oncotarget.13416
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MYC associated zinc finger protein (MAZ) plays a key role in regulation of gene expression and tumor development. Studies have shown that deregulated expression of MAZ is closely related to the progression of tumors such as glioblastoma, breast cancer, prostate cancer and liposarcoma. However, the role of MAZ in hepatocellular carcinoma (HCC) has not been fully elucidated. Here, we found that expression of MAZ was increased in HCC and correlated to the distant metastasis of HCC. Moreover, we found that MAZ had a relationship with zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), two important mesenchymal markers in epithelial-mesenchymal transition (EMT) that were over-expressed in HCC. After knocking-down MAZ expression in HCC cell lines using RNA interruption, HCC cell proliferation, tumorigenesis, invasion and migration were significantly inhibited. In addition, we found that expression of other EMT markers was also changed besides ZEB1 and ZEB2 by decreasing MAZ expression, both detected in vivo and in vitro assays. Therefore, we conclude that MAZ can promote the invasion and metastasis of HCC by inducing EMT.
引用
收藏
页码:86420 / 86432
页数:13
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