TAB3 upregulates Survivin expression to promote colorectal cancer invasion and metastasis by binding to the TAK1-TRAF6 complex

被引:10
|
作者
Luo, Chen [1 ,2 ]
Yuan, Rongfa [1 ,2 ]
Chen, Leifeng [1 ,2 ]
Zhou, Wei [3 ]
Shen, Wei [1 ]
Qiu, Yumin [1 ,2 ]
Shao, Jun [1 ,2 ]
Yan, Jinlong [1 ,2 ]
Shao, Jianghua [1 ,2 ]
机构
[1] Nanchang Univ, Dept Gen Surg, Affiliated Hosp 2, Nanchang 330006, Jiangxi, Peoples R China
[2] Jiangxi Prov Key Lab Mol Med, Nanchang 330006, Jiangxi, Peoples R China
[3] Jiangxi Prov Canc Hosp, Dept Gastrointestinal Surg, Nanchang 330029, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
TAB3; Survivin; NF-kappa B pathway; colorectal cancer; metastasis; NF-KAPPA-B; BETA-CATENIN; TGF-BETA; CELLS; TAK1; PROTEIN; ACTIVATION; OVEREXPRESSION; INHIBITION; CARCINOMA;
D O I
10.18632/oncotarget.22497
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Transforming growth factor-beta-activated kinase 1 (TAK1)-binding protein 3 (TAB3) is involved in cancer proliferation and metastasis, but its role in colorectal cancer remains unclear. In this study, we demonstrated that TAB3 is upregulated in colorectal cancer tissues and that high TAB3 levels correlated with tumor metastasis and a poor prognosis in colorectal cancer. In addition, TAB3 knockdown decreased Survivin expression and suppressed colorectal cancer cell migration and invasion in vitro, and reduced liver metastasis in vivo. Importantly, we found that TAB3 regulated Survivin expression by activating the NF-kappa B pathway through the formation of the TAK1-TAB3-TRAF6 complex. These findings suggest TAB3 may be a useful prognostic biomarker in colorectal cancer and a target for treatment of metastatic colorectal cancer.
引用
收藏
页码:106565 / 106576
页数:12
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