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Overexpression of UBR5 promotes tumor growth in gallbladder cancer via PTEN/PI3K/Akt signal pathway
Author(s) -
Zhang Zhen,
Zheng Xin,
Li Jiaxin,
Duan Jutao,
Cui Lihua,
Yang Lei,
Zhang Lanqiu,
Zhang Qi,
Wang Ximo
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28431
Subject(s) - pten , cancer research , protein kinase b , tensin , pi3k/akt/mtor pathway , ubiquitin ligase , gallbladder cancer , cell growth , biology , ubiquitin , gene knockdown , proteasome , cancer , phosphorylation , signal transduction , microbiology and biotechnology , apoptosis , biochemistry , genetics , gene
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.