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Open Access Research article

PRAF3 induces apoptosis and inhibits migration and invasion in human esophageal squamous cell carcinoma

Guo-Zhen Shi2, Yang Yuan1, Guo-Jun Jiang2, Zhi-Jun Ge3, Jian Zhou3, De-Jun Gong1, Jing Tao1, Yong-Fei Tan25* and Sheng-Dong Huang14*

Author Affiliations

1 Institute of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, PR China

2 Department of Cardiothoracic Surgery, Yixing People's Hospital, Jiangsu, PR, China

3 Department of Pathology, Yixing People's Hospital, Jiangsu, PR China

4 Institute of Cardiothoracic Surgery, Changhai Hospital, 168, Changhai Rd, Shanghai, PR China

5 Institute of Cardiothoracic Surgery, Yixing People's Hospital, 75 Tongzhenguan Rd, Wuxi, Jiangsu, PR China

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BMC Cancer 2012, 12:97  doi:10.1186/1471-2407-12-97

Published: 21 March 2012

Abstract

Background

Prenylated Rab acceptor 1 domain family member 3 (PRAF3) is involved in the regulation of many cellular processes including apoptosis, migration and invasion. This study was conducted to investigate the effect of PRAF3 on apoptosis, migration and invasion in human esophageal squamous cell carcinoma (ESCC).

Methods

The expression of PRAF3 mRNA and protein in primary ESCC and the matched normal tissues (57cases) was determined by quantitative RT-PCR and Western blot. Immunohistochemical analysis of PRAF3 expression was carried out in paraffin-embedded sections of ESCC and correlated with clinical features. The role of PRAF3 in apoptosis, migration and invasion was studied in ESCC cell lines of Eca109 and TE-1 through the adenovirus mediated PRAF3 gene transfer. The effect of PRAF3 on apoptosis was analyzed by annexin V-FITC assay. The regulation of PRAF3 on migration was determined by transwell and wounding healing assay, while the cellular invasion was analyzed by matrigel-coated transwell assay.

Results

We found that the expression of PRAF3 was significantly down-regulated in ESCC tissue compared with the matched normal tissue and was correlated with the clinical features of pathological grade, tumor stage and lymph node metastasis. Moreover, overexpression of PRAF3 induced cell apoptosis through both caspase-8 and caspase-9 dependent pathways, and inhibited cell migration and invasion by suppressing the activity of both MMP-2 and MMP-9 in human ESCC cell lines.

Conclusions

Our data suggest that PRAF3 plays an important role in the regulation of tumor progression and metastasis and serves as a tumor suppressor in human ESCC. We propose that PRAF3 might be used as a potential therapeutic agent for human ESCC.