Inhibition of PRL-3 gene expression in gastric cancer cell line SGC7901 via microRNA suppressed reduces peritoneal metastasis

被引：144

作者：

Li, Zhengrong ^{[1
]}

Zhan, Wenhua ^{[1
]}

Wang, Zhao ^{[1
]}

Zhu, Baohe ^{[1
]}

He, Yulong ^{[1
]}

Peng, Junsheng ^{[1
]}

Cai, Shirong ^{[1
]}

Ma, Jinping ^{[1
]}

机构：

[1] Sun Yat Sen Univ, Dept Gastrointestinopancreat Surg, Affiliated Hosp 1, Gastr Ctr, Guangzhou 510080, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 348卷 / 01期

基金：

中国国家自然科学基金;

关键词：

PRL-3; gastric cancer; peritoneal metastasis; RNA interference; microRNA; plasmid vector;

D O I：

10.1016/j.bbrc.2006.07.043

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

High expression of PRL-3, a protein tyrosine phosphatase, is proved to be associated with lymph node metastasis in gastric carcinoma from previous studies. In this paper, we examined the relationship between PRL-3 expression and peritoneal metastasis in gastric carcinoma. We applied the artificial miRNA (pCMV-PRL3miRNA), which is based on the murine miR-155 sequence, to efficiently silence the target gene expression of PRL-3 in SGC7901 gastric cancer cells at both mRNA and protein levels. Then we observed that, in vitro, pCMV-PRL3miRNA significantly depressed the SGC7901 cell invasion and migration independent of cellular proliferation. In vivo, PRL-3 knockdown effectively suppressed the growth of peritoneal metastases and improved the prognosis in nude mice. Therefore, we concluded that artificial miRNA can depress the expression of PRL-3, and that PRL-3 might be a potential therapeutic target for gastric cancer peritoneal metastasis. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：229 / 237

页数：9

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