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Decreased expression of SLC39A14 is associated with tumor aggressiveness and biochemical recurrence of human prostate cancer

Authors Xu X, Wang C, Zhu Y, Chen W, Shao S, Jiang F, Liao Q

Received 5 January 2016

Accepted for publication 13 April 2016

Published 11 July 2016 Volume 2016:9 Pages 4197—4205


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Narasimha Reddy Parine

Peer reviewer comments 3

Editor who approved publication: Professor Min Li

Xiao-Ming Xu,1,2 Cheng-Gong Wang,1 Yu-Di Zhu,2 Wei-Hua Chen,3 Si-Liang Shao,2 Fu-Neng Jiang,4 Qian-De Liao1

1Xiangya Hospital, Central South University, Changsha, Hunan, 2Department of Urology, Ningbo No 2 Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang, 3Shanghai East Hospital, Tongji University, Shanghai, 4Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People’s Hospital, Guangzhou Medical University, Guangzhou, People’s Republic of China

Objective: Solute carrier family 39, member 14 (SLC39A14), has been identified as a potential biomarker for various cancers. However, its roles in prostate cancer (PCa) are still unclear. The aim of this study was to investigate the clinical significance of SLC39A14 in patients with PCa and its functions in malignant phenotypes of PCa cells.
Patients and methods: Subcellular localization and expression pattern of SLC39A14 protein were examined by immunohistochemistry. Then, the associations of SLC39A14 expression with various clinicopathological features and clinical outcome of patients with PCa were statistically evaluated. Subsequently, the effects of SLC39A14 overexpression and knockdown on PCa cell proliferation and motility were, respectively, examined by Cell Counting Kit-8, transwell, and wound-healing assays.
Results: The immunoreactive scores of SLC39A14 protein in human PCa tissues were significantly lower than those in normal prostate tissues. Based on the Taylor dataset, SLC39A14 downregulation occurred more frequently in patients with PCa with a higher Gleason score (P<0.001), advanced clinical stage (P=0.008), presence of metastasis (P=0.009), and prostate-specific antigen failure (P=0.006). More interestingly, the survival analysis identified SLC39A14 as an independent factor for predicting the biochemical recurrence-free survival of patients with PCa (P=0.017). Functionally, the enforced expression of SLC39A14 could suppress cell proliferation, invasion, and migration of PCa cell lines in vitro, which could be reversed by the knockdown of SLC39A14.
Conclusion: Decreased expression of SLC39A14 may lead to malignant phenotypes of PCa cells and aggressive tumor progression in patients with PCa. Importantly, SLC39A14 may function as a tumor suppressor and a biomarker for screening patients with biochemical recurrence following radical prostatectomy.

Keywords: prostate cancer, solute carrier family 39 member 14, biochemical recurrence-free survival, tumor suppressor

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