期刊
ONCOGENE
卷 28, 期 32, 页码 2910-2918出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2009.148
关键词
PAR-3; PARD3; esophageal squamous cell carcinoma; homozygous deletion; tight junction; metastasis
资金
- Japan Society for the Program of Science [18390223, 20590408]
- Grants-in-Aid for Scientific Research [18390223, 20590408] Funding Source: KAKEN
The partition-defective 3 (PAR-3) protein is implicated in the formation of tight junctions at epithelial cell-cell contacts. We investigated DNA copy number aberrations in human esophageal squamous cell carcinoma (ESCC) cell lines using a high-density oligonucleotide microarray and found a homozygous deletion of PARD3 (the gene encoding PAR-3). Exogenous expression of PARD3 in ESCC cells lacking this gene enhanced the recruitment of zonula occludens 1 (ZO-1), a marker of tight junctions, to sites of cell-cell contact. Conversely, knockdown of PARD3 in ESCC cells expressing this gene caused a disruption of ZO-1 localization at cell-cell borders. A copy number loss of PARD3 was observed in 15% of primary ESCC cells. Expression of PARD3 was significantly reduced in primary ESCC tumors compared with their nontumorous counterparts, and this reduced expression was associated with positive lymph node metastasis and poor differentiation. Our results suggest that deletion and reduced expression of PARD3 may be a novel mechanism that drives the progression of ESCC. Oncogene (2009) 28, 2910-2918; doi:10.1038/onc.2009.148; published online 8 June 2009
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据