Oncotarget

Research Papers:

Identification of glycerol-3-phosphate dehydrogenase 1 as a tumour suppressor in human breast cancer

Cefan Zhou, Jing Yu, Ming Wang, Jing Yang, Hui Xiong, Huang Huang, Dongli Wu, Shimeng Hu, Yefu Wang, Xing-Zhen Chen and Jingfeng Tang _

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Oncotarget. 2017; 8:101309-101324. https://doi.org/10.18632/oncotarget.21087

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Abstract

Cefan Zhou1,2, Jing Yu2,3, Ming Wang4, Jing Yang5, Hui Xiong6, Huang Huang1, Dongli Wu2, Shimeng Hu2, Yefu Wang2, Xing-Zhen Chen1,7 and Jingfeng Tang1

1Institute of Biomedical and Pharmaceutical Sciences, Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei Provincial Cooperative Innovation Center of Industrial Fermentation, Hubei Key Laboratory of Industrial Microbiology, Hubei University of Technology, Wuhan, Hubei, China

2The State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, Hubei, China

3Department of Clinical Laboratory, Hubei Cancer Hospital, Wuhan, Hubei, China

4Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan, Hubei, China

5Institute for Immunology, Tsinghua University, Beijing, China

6XiLi People's Hospital, Shenzhen, Guangdong, China

7Membrane Protein Disease Research Group, Department of Physiology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada

Correspondence to:

Jingfeng Tang, email: Jingfeng_HUT@163.com

Keywords: prognostic significance, biomarker, cell proliferation, survival, meta-analysis

Received: July 05, 2017     Accepted: August 27, 2017     Published: September 19, 2017

ABSTRACT

In the present study, we found the mRNA expression level of glycerol-3-phosphate dehydrogenase (GPD1) was significantly downregulated in human breast cancer patients. Patients with reduced GPD1 expression exhibited poorer overall metastatic relapse-free survival (p = 0.0013). Further Cox proportional hazard model analysis revealed that the reduced expression of GPD1 is an independent predictor of overall survival in oestrogen receptor-positive (p = 0.0027, HR = 0.91, 95% CI = 0.85–0.97, N = 3,917) and nodal-negative (p = 0.0013, HR = 0.87, 95% CI = 0.80–0.95, N = 2,456) breast cancer patients. We also demonstrated that GPD1 was a direct target of miR-370, which was significantly upregulated in human breast cancer. We further showed that exogenous expression of GPD1 in human MCF-7 and MDA-MB-231 breast cancer cells significantly inhibited cell proliferation, migration, and invasion. Our results, therefore, suggest a novel tumour suppressor function for GPD1 and contribute to the understanding of cancer metabolism.


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