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Published in: Tumor Biology 10/2016

01-10-2016 | Original Article

Downregulation of paraoxonase 3 contributes to aggressive human hepatocellular carcinoma progression and associates with poor prognosis

Authors: Yuepeng Jin, Qiang Li, Junjun Qiu, Xiufen Zhao, Chunxiao Zheng, Shixu Lv, Yongyu Bai, Yunfeng Shan, Le-chi Ye

Published in: Tumor Biology | Issue 10/2016

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Abstract

Paraoxonase (PON) enzymes possess antioxidant properties and protect against cardiovascular diseases. As a member of PON family, PON3 is primarily synthesized in the liver and poorly investigated. This study aimed to examine the expression of PON3 in human hepatocellular carcinoma (HCC) and investigate the clinical significance and biological function of PON3 in HCC patients. We first analyzed PON3 expression in 50 paired HCC samples (HCC tissues vs matched para-cancerous tissues) and 160 clinical HCC specimens by using immunohistochemistry (IHC). Our results showed that the expression of PON3 was downregulated in HCC and significantly associated with tumor-node-metastasis (TNM) stage, tumor size, and tumor number. Kaplan-Meier survival and Cox regression analyses showed that PON3 was an independent prognostic factor for overall survival (OS) and time to recurrence (TTR). Finally, we aimed to reveal the biological function of PON3 in HCC growth and metastasis, and our results showed that overexpression of PON3 potently inhibited growth and metastasis of HCC. Collectively, our study demonstrated that PON3 exhibited tumor-suppressive effects toward HCC and it might serve as a novel prognostic marker in HCC.
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Metadata
Title
Downregulation of paraoxonase 3 contributes to aggressive human hepatocellular carcinoma progression and associates with poor prognosis
Authors
Yuepeng Jin
Qiang Li
Junjun Qiu
Xiufen Zhao
Chunxiao Zheng
Shixu Lv
Yongyu Bai
Yunfeng Shan
Le-chi Ye
Publication date
01-10-2016
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 10/2016
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-016-5247-z

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