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

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          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.

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          Author and article information

          Journal
          J Cell Biochem
          Journal of cellular biochemistry
          Wiley
          1097-4644
          0730-2312
          Feb 18 2019
          Affiliations
          [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.
          Article
          10.1002/jcb.28431
          30775814
          481893d1-6f31-4e54-afa5-4d019fb0c52b
          © 2019 Wiley Periodicals, Inc.
          History

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

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