Protein phosphatase magnesium-dependent 1δ is a novel tumor marker and target in hepatocellular carcinoma

Abstract

Hepatocellular carcinoma (HCC) is a lethal liver malignancy worldwide. In this study, we reported that protein phosphatase magnesium-dependent 1δ (PPM1D) was highly expressed in the majority of HCC cases (approximately 59%) and significantly associated with high serum α-fetoprotein (AFP) level (P= 0.044). Kaplan-Meier and Cox regression data indicated that PPM1D overexpression was an independent predictor of HCC-specific overall survival (HR, 2.799; 95% CI, 1.346–5.818, P = 0.006). Overexpressing PPM1D promoted cell viability and invasion, whereas RNA interference-mediated knockdown of PPM1D inhibited proliferation, invasion, and migration of cultured HCC cells. In addition, PPM1D suppression by small interfering RNA decreased the tumorigenicity of HCC cells in vivo. Overall, results suggest that PPM1D is a potential prognostic marker and therapeutic target for HCC.

Keywords

PPM1D / hepatocellular carcinoma / prognosis / target therapy

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Acknowledgements

This study was supported by grants from the National Natural Science Foundation of China (Nos. 81000880 and 81370057 to Zhi Xu), the Key Project supported by Medical Science and Technology Development Foundation, Nanjing Department of Health (JQX12007 to Zhi Xu), the clinical special project for Natural Science Foundation of Jiangsu Province (BL2012016 to Jinfei Chen), and the Nanjing 12th Five-Year Key Scientific Project of Medicine to Jinfei Chen.

Compliance with ethics guidelines

Zhi Xu, Chunxiang Cao, Haiyan Xia, Shujing Shi, Lingzhi Hong, Xiaowei Wei, Dongying Gu, Jianmin Bian, Zijun Liu, Wenbin Huang, Yixin Zhang, Song He, Nikki Pui-Yue Lee, and Jinfei Chen declare that they have no conflict of interest. The study was approved by the institutional review board of Nantong Tumor Hospital and Nanjing Medical University (Nanjing, China). Enrolled patients provided signed informed consents on using the collected specimens for medical research.

Electronic Supplementary MaterialƒSupplementary material is available in the online version of this article at http://dx.doi.org/10.1007/s11684-016-0433-3 and is accessible for authorized users.

RIGHTS & PERMISSIONS

2016 Higher Education Press and Springer-Verlag Berlin Heidelberg