Oncotarget

Research Papers:

This article has been corrected. Correction in: Oncotarget. 2017; 8:30617-18.

PRSS8 methylation and its significance in esophageal squamous cell carcinoma

Yonghua Bao, Qian Wang, Yongchen Guo, Zhiguo Chen, Kai Li, Yiqiong Yang, Huijuan Zhang, Huali Dong, Kui Shen and Wancai Yang _

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Oncotarget. 2016; 7:28540-28555. https://doi.org/10.18632/oncotarget.8677

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Abstract

Yonghua Bao1, Qian Wang2, Yongchen Guo1, Zhiguo Chen3, Kai Li4, Yiqiong Yang1, Huijuan Zhang3, Huali Dong5, Kui Shen5, Wancai Yang1,5

1Department of Pathology and Institute of Precision Medicine, Jining Medical University, Jining 272067, China

2Department of Immunology, Xinxiang Medical University, Xinxiang 453003, China

3Department of Pathology, Xinxiang Medical University, Xinxiang 453003, China

4Department of Pathology, The First Affiliated Hospital, Xinxiang Medical University, Xinxiang 453003, China

5Department of Pathology, University of Illinois at Chicago, Chicago, IL 60612, USA

Correspondence to:

Wancai Yang, email: [email protected]

Keywords: PRSS8, methylation, esophageal cancer, survival, cancer stroma

Received: December 20, 2015     Accepted: March 28, 2016     Published: April 11, 2016

ABSTRACT

Esophageal cancer is one of the most common cancers worldwide, and the incidence and mortality is increasing rapidly in recent years in China, but the underlying mechanisms are largely unclear. Herein we found that the expression of PRSS8, a serine protease prostasin, is significantly decreased in esophageal squamous cell carcinomas (ESCC) at mRNA and protein levels. The reduction of PRSS8 was well correlated with poor differentiation and shorter survival time. Interestingly, ESCC stromal expression of PRSS8 was significantly correlated with stromal lymphocyte infiltration and cancer progression. Methylation specific PCR showed that PRSS8 was hypermethylated in ESCC tissues and ESCC cell lines, which was linked to the downregulation of PRSS8 expression and decreased activities of PRSS8 promoter. De-methylation agent decitabine was able to restore PRSS8 expression, leading to the inhibition of cancer cell proliferation, motility, migration and cell cycle arrest. However, the restored PRSS8 and its tumor inhibition could be reversed by small interfering RNA targeting PRSS8. Mechanistic study showed that tumor inhibition of PRSS8 may be associated with proliferation- and epithelial mesenchymal transition - related proteins in ESCC cells. In conclusion, our finding showed that PRSS8 methylation and its stromal expression had important clinical significance in ESCC.


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