Decreased TSPAN1 promotes prostate cancer progression and is a marker for early biochemical recurrence after radical prostatectomy
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Fan Xu1,*, Yujing Gao2,*, Yanqing Wang1,*, Jiahua Pan1,*, Jianjun Sha1, Xiaoguang Shao1, Xunlei Kang3, Jun Qin1,4,5, M. James You6,7, Yiran Huang1, Baijun Dong1, Wei Xue1
1Department of Urology, RenJi Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
2Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Department of Biochemistry and Molecular Biology, Ningxia Medical University, Yinchuan, Ningxia, China
3Division of Oncology, Department of Medicine, University of Missouri School of Medicine, Columbia, MO, USA
4Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
5Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA
6Program of Genes and Development, The University of Texas Graduate School of Biomedical Sciences, Houston, TX, USA
7Department of Hematopathology, Division of Pathology and Laboratory Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
*These authors have contributed equally to this work
Baijun Dong, email: [email protected]
Wei Xue, email: [email protected]
Keywords: prostate cancer, TSPAN1, progression, prognosis, biochemical recurrence
Received: April 13, 2016 Accepted: August 10, 2016 Published: August 20, 2016
Patients with prostate cancer (PCa) have a variable prognosis. It is challenging to recognize the progressive disease. In this study, we focused on TSPAN1, a new member of the tetraspanin family. Its expression was decreased in progressive PCa and was an independent prognosis factor of biochemical recurrence after radical prostatectomy. In vitro, knockdown and overexpression of TSPAN1 in PCa cell lines showed that TSPAN1 could inhibit cell proliferation and migration. TSPAN1 was positive related to PTEN in both clinical specimen and mouse models. The combination of these two markers could increase their prognosis value especially in low risk patients. In vitro TSPAN1 knockdown resulted in increased Akt phosphorylation and caused evident cell cycle transition from G1 to S phase. Our data suggests that TSPAN1 is a valuable marker to recognize more progressive PCa.
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