Research Papers:

PAQR3 suppresses the proliferation, migration and tumorigenicity of human prostate cancer cells

Wenqiang Huang, Weiwei Guo, Xue You, Yi Pan, Zhenyang Dong, Gaozhen Jia, Chenghua Yang and Yan Chen _

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Oncotarget. 2017; 8:53948-53958. https://doi.org/10.18632/oncotarget.9807

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Wenqiang Huang1,*, Weiwei Guo1,*, Xue You1,2, Yi Pan1, Zhenyang Dong3, Gaozhen Jia3, Chenghua Yang1,4, Yan Chen1,2

1Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China

2School of Life Sciences and Technology, Shanghai Tech University, Shanghai, 200031, China

3Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, 200433, China

4Joint Center for Translational Research of Chronic Diseases, Shanghai Changhai Hospital, Second Military Medical University, Shanghai 2000433, China

*These authors contributed equally to this work

Correspondence to:

Yan Chen, email: [email protected]

Chenghua Yang, email: [email protected]

Keywords: human prostate cancer, PAQR3, cell proliferation, cell migration, tumor xenograft

Received: February 20, 2016     Accepted: May 28, 2016     Published: June 03, 2016


As a newly discovered tumor suppressor, the potential function of PAQR3 in human prostate cancer has not been demonstrated. In this study, we report that PAQR3 is able to inhibit the growth and migration of human prostate cancer cells both in vitro and in vivo. Overexpression of PAQR3 inhibits the proliferation of PC3 and DU145 cells by both MTT and colony formation assays. Consistently, knockdown of PAQR3 enhances the proliferation of these cells. In wound-healing and transwell assays, overexpression of PAQR3 reduces the migration of PC3 and DU145 cells, while PAQR3 knockdown increases it. In a tumor xenograft model, overexpression of PAQR3 suppresses tumor growth of PC3 cells in vivo, while PAQR3 knockdown promotes the tumor growth. PAQR3 is also able to inhibit serum-induced phosphorylation of AKT and ERK in both PC3 and DU145 cells. In addition, PAQR3 suppresses the expression of epithelial-mesenchymal transition (EMT) markers in PC3 cells. Collectively, these data indicate that PAQR3 has a tumor suppressive activity in human prostate cancer cells and may stand out as a potential therapeutic target for prostate cancers.

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