NF‐κBP65 promotes invasion and metastasis of oesophageal squamous cell cancer by regulating matrix metalloproteinase‐9 and epithelial‐to‐mesenchymal transition. (7th May 2013)

• Record Type: Journal Article
• Authors: Wang, Feng; He, Wei; Fanghui, Peng; Wang, Liuxing; Fan, Qingxia
• Is Part Of: Cell biology international. Volume 37:Number 8(2013)
• Page Start: 780
• Page End: 788
• Publication Date: 2013-05-07
• Subjects: Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10089
• Languages: English
• ISSNs: 1065-6995

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10089-sec-0001" sec-type="section"> <p>NF‐κB has been recognized as one of the factors responsible for the development of cancer; however, the mechanism by which high expression of NF‐κB contributes to the progression of human oesophageal squamous cell cancer (ESCC) is not fully understood. In our investigations, NF‐κBP65 was overexpressed in human ESCC tissues, especially in ESCC tissues with deep invasion and lymph node metastasis. Suppression of NF‐κBP65 by siRNA decreased the invasion and proliferation ability of EC9706 cells in vitro. Furthermore, siRNA‐mediated NF‐κBP65 knock‐down could lead to the downregulation of MMP‐9, a metastasis‐related gene. Reduced E‐cadherin is a hallmark of invasive carcinomas that have acquired epithelial–mesenchymal transition (EMT) phenotypes and Vimentin is another molecule that is used widely as a marker of the EMT. We found upregulation of E‐cadherin expression and downregulation of Vimentin was induced by NF‐κBP65 siRNA, which suggests that NF‐κBP65 siRNA could inhibit the invasion and proliferation ability of ECSS through attenuating the expression of MMP‐9 and EMT. Thus, ESCC NF‐κBP65 could be a useful target for cancer prevention and therapy.</p> </sec> </abstract>