Oncotarget

Research Papers:

PLD1 overexpression promotes invasion and migration and function as a risk factor for Chinese glioma patients

Wenjun Tang, Richu Liang, Yonghong Duan, Qiaoling Shi, Xiaofei Liu and Yongshi Liao _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:57039-57046. https://doi.org/10.18632/oncotarget.18961

Metrics: PDF 1750 views  |   HTML 1942 views  |   ?  


Abstract

Wenjun Tang1,*, Richu Liang1,*, Yonghong Duan1, Qiaoling Shi1, Xiaofei Liu1 and Yongshi Liao1

1Department of Neurosurgery, The Second Hospital Affiliated to University of South China, Hengyang, Hunan, 421000 China

*These authors contributed equally to this work

Correspondence to:

Yongshi Liao, email: [email protected]

Keywords: PLD1, glioma, prognosis, invasion, migration

Received: January 16, 2017     Accepted: June 18, 2017     Published: July 05, 2017

ABSTRACT

Glioma is a lethal disease with few effective therapeutic options. Recently, insights into cancer biology had suggested that abnormal lipid metabolism was a risk factor for various human malignancies, including glioma. As a key enzyme implicated in lipid metabolism, PLD1 was overexpression in multiple human cancers, and it was stated to be responsible for aggressive phenotypes, such as angiogenesis and chemoresistance. However, there was still much to know about its expression and function in glioma. In the present study, we showed that PLD1 was overexpression in clinical samples of glioma. In addition, the correlation assay revealed that PLD1 overexpression was correlated with poor differentiation (p = 0.04), and it was responsible for a poor prognosis for the patients (p = 0.009). Furthermore, we showed in COX regression assay that PLD1 was a risk factor for glioma (p = 0.018, HR = 0.461, 95% CI = 0.243–0.887). Consistently, we found that PLD1 was overexpression in glioma cell lines, and it could facilitate the proliferation and migration. Taken together, our study suggested that PLD1 was pro-tumoral in glioma, and that further studies were urgently needed so as to define whether it was a novel therapeutic target for the disease.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 18961