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J Cell Biochem. 2019 Feb 18. doi: 10.1002/jcb.28431. [Epub ahead of print]

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

Author information

1
Department of Gastrointestinal Surgery, Peking University People's Hospital, Beijing, China.
2
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Institute of Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin, China.
3
Graduate School of Tianjin Medical University, Tianjin, China.
4
Department of Minimal Invasive Surgery, Tianjin Nankai Hospital, Tianjin, China.

Abstract

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.

KEYWORDS:

gallbladder cancer; phosphatase and tensin homolog; proliferation; tumor growth; ubiquitin protein ligase E3 component N-recognin 5

PMID:
30775814
DOI:
10.1002/jcb.28431

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