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Gene silencing of beta-catenin by RNAi inhibits cell proliferation in human esophageal cancer cells in vitro and in nude mice.

Abstract：

:beta-Catenin, which is frequently overexpressed in a variety of human cancers including esophageal cancer, mediates cancer cell proliferation and tumor growth. In the present study, we used a human U6 promoter-driven DNA-template approach to induce short hairpin RNA (shRNA)-triggered RNA interference to silence beta-catenin gene expression in human esophageal squamous cell carcinoma cell line Eca-109, and then evaluated its effects on the proliferation and growth of tumor cells in vitro and in nude mice. beta-Catenin expression levels decreased markedly in Eca-109 cells transfected with a plasmid expressing shRNA for beta-catenin. Downregulation of beta-catenin was concomitantly accompanied by reduction of cyclin D1, colony formation, and growth inhibition of Eca-109 cells in vitro. The mechanism appears to be the G0/G1 phase arrest but not induction of apoptosis. In vivo, treatment of Eca-109 cells with beta-catenin shRNA greatly impeded tumor growth in nude mice. We conclude that plasmid vector-mediated beta-catenin RNA interference holds great promise as a novel treatment on human esophageal cancer with beta-catenin overexpression.

journal_name

Dis Esophagus

journal_title

Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus

authors

Wang JS,Zheng CL,Wang YJ,Wen JF,Ren HZ,Liu Y,Jiang HY

doi

10.1111/j.1442-2050.2008.00875.x

subject

Has Abstract

pub_date

2009-01-01 00:00:00

pages

151-62

issue

2

eissn

1120-8694

issn

1442-2050

pii

DES875

journal_volume

22

pub_type

杂志文章

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