A novel oncogene TRIM63 promotes cell proliferation and migration via activating Wnt/β-catenin signaling pathway in breast cancer

被引:17
|
作者
Li, Kai [2 ]
Pan, Wenting [2 ]
Ma, Yanbin [2 ]
Xu, Xiaolong [2 ]
Gao, Yang [2 ]
He, Yanqi [2 ]
Wei, Lei [2 ]
Zhang, Jingwei [1 ]
机构
[1] Wuhan Univ, Dept Breast & Thyroid Surg, Zhongnan Hosp, Hubei Key Lab Tumor Biol Behav,Hubei Canc Clin St, 169 Donghu Rd, Wuhan 430071, Hubei, Peoples R China
[2] Wuhan Univ, Dept Pathol & Pathophysiol, Hubei Prov Key Lab Dev Originated Dis, Sch Basic Med Sci, Wuhan 430071, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
TRIM63; Wnt/beta-catenin signaling pathway; Cell proliferation; Cell migration; Breast cancer; PROTEINS; INHIBITION; MURF1;
D O I
10.1016/j.prp.2019.152573
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The development of breast cancer is still a relatively unclear biological process, and there is currently no consensus on the occurrence of breast cancer and the process of tumor metastases. This study was to reveal a correlation between TRIM63 and the development of breast cancer. In this study, we found that the expression of TRIM63 was significantly increased in breast cancer tissues and closely related to pathological differentiation and TNM stage of breast cancer. Overexpression of TRIM63 could significantly promote proliferation and migration of breast cancer cells, while TRIM63 knockdown significantly inhibited the proliferation and migration of breast cancer cells. In addition, TRIM63 could activate Wnt/beta-catenin signaling pathway in breast cancer cells. Further study found that TRIM63 could regulate beta-catenin degradation by promoting GSK3 beta phosphorylation. Our study revealed that TRIM63, as an oncogene, involved in breast cancer progression by activating the Wnt/beta-catenin signaling pathway, suggesting that the potential applicability of TRIM63 as a target for breast cancer treatment.
引用
收藏
页数:7
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