详细信息

Knockdown of protein tyrosine phosphatase receptor U inhibits growth and motility of gastric cancer cells  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Knockdown of protein tyrosine phosphatase receptor U inhibits growth and motility of gastric cancer cells

作者:Liu, Yongjie[1];Zhu, Zhichuan[1];Xiong, Zhiqi[1];Zheng, Jing[1];Hui, Zelan[1];Qiu, Jiangfeng[2]

机构:[1]E China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, Shanghai 200237, Peoples R China;[2]Ningbo First Hosp, Dept Gastrointestinal Surg, Ningbo 315010, Zhejiang, Peoples R China

年份:2014

卷号:7

期号:9

起止页码:5750

外文期刊名:INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000345129400035)】;

基金:This work was supported by grants from the National Natural Science Foundation of China (No. 31300904) and the Ningbo Natural Science Foundation (No. 2012A610209). The authors appreciate the International Postdoctoral Exchange Fellowship Program China (20130018) for the financial support of this work.

语种:英文

外文关键词:PTPRU; gastric cancer; proliferation; motility; beta-catenin

摘要:Protein tyrosine phosphatase receptor U (PTPRU) has been shown to be a tumor suppressor in colon cancer by dephosphorylating beta-catenin and reducing the activation of beta-catenin signaling. Here, we investigate the expression of PTPRU protein in gastric cancer cell lines, gastric cancer tissues and respective adjacent non-cancer tissues and find that the 130kDa nuclear-localized PTPRU fragment is the main PTPRU isoform in gastric cancer cells, whereas the full-length PTPRU is relatively lowly expressed. The level of the 130kDa PTPRU is higher in gastric cancer tissues than in adjacent non-cancer tissues. Knockdown of endogenous PTPRU in gastric cancer cells using lentivirus-delivered specific shRNA results in the attenuation of cell growth, migration, invasion and adhesion. Knockdown of PTPRU also inhibits tyrosine phosphorylation and transcriptional activity of beta-catenin as well as levels of focal adhesion proteins and lysine methylation of histone H3. These results indicate that PTPRU is required for gastric cancer progression and may serve as a potential therapeutic target.

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