Regulatory mechanisms controlling human E-cadherin gene expression

Yan Nan Liu, Wen Wen Lee, Chun Yi Wang, Tung Hui Chao, Yvan Chen, Hshiung Chen Ji

研究成果: 雜誌貢獻文章同行評審

162 引文 斯高帕斯(Scopus)

摘要

In cancer cells, loss of E-cadherin gene expression caused dysfunction of the cell-cell junction system, triggering cancer invasion and metastasis. Therefore, E-cadherin is an important tumor-suppressor gene. To understand how E-cadherin gene expression is regulated in cancer cells, we have used E-cadherin-positive and -negative expressing cells to find out the possible up- or downregulating transcription factors in human E-cadherin regulatory sequences. Functional analysis of human E-cadherin regulatory sequences constructs indicated that AML1, Sp1, and p300 may play important roles in promoting E-cadherin expression. In addition, we found there are four HNF3-binding sites in human E-cadherin regulatory sequences. The exogenous HNF3 can enhance the E-cadherin promoter activity in metastatic breast cancer cells and the metastatic breast cancer cells stably transfected with HNF3 showed re-expression of E-cadherin. The HNF3 stable transfectants changed from mesenchymal-like into epithelial morphology. The trans-well assays showed the re-expressed E-cadherin reduced cell motility of metastatic breast cancer cells. These results suggested HNF3 may play important roles in the upregulation of the E-cadherin promoter, with the consequent re-expression of E-cadherin, thus reducing the metastatic potential of breast cancer cells. These findings suggested HNF3 plays important roles in the upregulation of the E-cadherin gene and may be able to reduce the motility of metastatic breast cancer cells.
原文英語
頁(從 - 到)8277-8290
頁數14
期刊Oncogene
24
發行號56
DOIs
出版狀態已發佈 - 12月 15 2005
對外發佈

ASJC Scopus subject areas

  • 分子生物學
  • 遺傳學
  • 癌症研究

指紋

深入研究「Regulatory mechanisms controlling human E-cadherin gene expression」主題。共同形成了獨特的指紋。

引用此