Overexpression of UBR5 promotes tumor growth in gallbladder cancer via PTEN/PI3K/Akt signal pathway

被引:19
|
作者
Zhang, Zhen [1 ,3 ]
Zheng, Xin [2 ,3 ]
Li, Jiaxin [2 ,3 ]
Duan, Jutao [4 ]
Cui, Lihua [3 ]
Yang, Lei [3 ]
Zhang, Lanqiu [3 ]
Zhang, Qi [3 ]
Wang, Ximo [3 ]
机构
[1] Peking Univ, Peoples Hosp, Dept Gastrointestinal Surg, Beijing, Peoples R China
[2] Tianjin Med Univ, Grad Sch, Tianjin, Peoples R China
[3] Tianjin Nankai Hosp, Inst Acute Abdominal Dis, Tianjin Key Lab Acute Abdomen Dis Associated Orga, Tianjin 300100, Peoples R China
[4] Tianjin Nankai Hosp, Dept Minimal Invas Surg, Tianjin, Peoples R China
基金
中国国家自然科学基金;
关键词
gallbladder cancer; proliferation; phosphatase and tensin homolog; tumor growth; ubiquitin protein ligase E3 component N-recognin 5; UBIQUITIN LIGASE UBR5; CELL-PROLIFERATION; PHOSPHORYLATION; METASTASIS; PTEN; GENE; EDD;
D O I
10.1002/jcb.28431
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
As a key regulator of the ubiquitin-proteasome system, ubiquitin protein ligase E3 component N-recognin 5 (UBR5) plays an important role in various cancers. In this study, our results showed for the first time that UBR5 was overexpressed in gallbladder cancer (GBC) tumor tissues. UBR5 overexpression was significantly associated with tumor size, histological and tumor differentiation. UBR5 overexpression was also associated with poor prognosis in patients with GBC. The knockdown of UBR5 remarkably inhibited the cell proliferation and colony formation of GBC-Shandong (SD) cells in vitro and in vivo. UBR5 potentially increases the level of protein kinase B phosphorylation via the degradation of phosphatase and tensin homolog, which contributes to tumor growth in GBC. UBR5 may be an important biomarker for predicting the prognosis of patients with GBC.
引用
收藏
页码:11517 / 11524
页数:8
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