Research Papers:

CtBP2 overexpression promotes tumor cell proliferation and invasion in gastric cancer and is associated with poor prognosis

Faxiang Dai, Yi Xuan, Jie-Jie Jin, Shengjia Yu, Zi-Wen Long, Hong Cai, Xiao-Wen Liu, Ye Zhou, Ya-Nong Wang, Zhong Chen and Hua Huang _

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Oncotarget. 2017; 8:28736-28749. https://doi.org/10.18632/oncotarget.15661

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Faxiang Dai1,2,3,*, Yi Xuan1,2,*, Jie-Jie Jin1,2,*, Shengjia Yu1,2, Zi-Wen Long1,2, Hong Cai1,2, Xiao-Wen Liu1,2, Ye Zhou1,2, Ya-Nong Wang1,2, Zhong Chen3, Hua Huang1,2

1Department of Gastric Cancer and Soft Tissue Sarcoma, Fudan University Shanghai Cancer Center, Shanghai 200032, China

2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China

3Department of Hepatobiliary Surgery, Affiliated Hospital of Nantong University, Jiangsu Province, Nantong 226001, China

*These authors have contributed equally to this work

Correspondence to:

Hua Huang, email: huahuang@fudan.edu.cn

Zhong Chen, email: chenz9806@163.com

Keywords: CtBP2, gastric cancer, prognosis

Received: June 29, 2016    Accepted: January 23, 2017    Published: February 24, 2017


C-terminal binding protein-2 (CtBP2), a transcriptional corepressor, has been reported to correlate with tumorigenesis and progression and predict a poor prognosis in several human cancers. However, few studies on CtBP2 in gastric cancer (GC) have been performed. In this research, we evaluated the correlations between CtBP2 expression and the clinicopathological characteristics, as well as prognosis of GC patients. The effects of silencing CtBP2 expression on GC cells biology activity were also assessed. The results showed that CtBP2 was overexpressed in GC tissues and closely correlated with poor differentiation, advanced tumor stage and poor prognosis in GC patients. CtBP2 induced epithelial-to-mesenchymal transition (EMT) and repressed PTEN to increase proliferation rate, migration, and invasion in GC cells. Silencing CtBP2 inhibited GC growth in nude mice model. In conclusion, CtBP2 is overexpressed in GC and may accelerate GC tumorigenesis and metastasis, which could represent an independent prognostic marker and promising therapeutic target for GC.

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