Research Papers:

Epigenetically downregulated Semaphorin 3E contributes to gastric cancer

Hui Chen, Guo-Hua Xie, Wei-Wei Wang, Xiang-Liang Yuan, Wen-Ming Xing, Hong-Jing Liu, Jin Chen, Min Dou and Li-Song Shen _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2015; 6:20449-20465. https://doi.org/10.18632/oncotarget.3936

Metrics: PDF 2209 views  |   HTML 2119 views  |   ?  


Hui Chen1, Guo-Hua Xie1, Wei-Wei Wang1, Xiang-Liang Yuan1, Wen-Ming Xing2, Hong-Jing Liu1, Jin Chen1, Min Dou1, Li-Song Shen1

1Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China

2Department of Academy, Shanghai Association for Science & Technology, Shanghai 200020, China

Correspondence to:

Li-Song Shen, e-mail: [email protected]

Keywords: Sema3E, gastric cancer, epigenetics, proliferation, migration

Received: January 23, 2015     Accepted: April 29, 2015     Published: May 12, 2015


Axon guidance protein Semaphorin 3E (Sema3E) promotes tumor metastasis and suppresses tumor cell death. Here, we demonstrated that Sema3E was decreased in gastric cancer. Its levels were inversely associated with tumor progression. Levels of Sema3E were associated with low p300 and high class I histone deacetylase (class I HDAC). Ectopic expression of Sema3E inhibited proliferation and colony formation of gastric cancer cell lines in vitro and xenografts in vivo. Sema3E overexpression inhibited migration and invasion of gastric cancer cells, which was associated with induction of E-cadherin and reduction of Akt and ERK1/2 phosphorylation. We suggest that silencing of Sema3E contributes to the pathogenesis of gastric cancer.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 3936