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Suppression of growth and increased cellular attachment after expression of DAL-1 in MCF-7 breast cancer cells.

Abstract
The differentially expressed in adenocarcinoma of the lung (DAL-1) gene, which shares significant homology with members of the 4.1/ezrin/radixin/moesin/neurofibromatosis 2 (ERM/NF2) protein family, has previously been shown to suppress growth in lung cancer cell lines. This gene localizes to chromosome band 18p11.3, which undergoes loss of heterozygosity (LOH) in nonsmall cell lung carcinomas and a significant proportion of ductal carcinomas in situ (DCIS) of the breast. This finding suggests that alteration of gene(s) (possibly DAL-1) within this chromosomal region may be important early in the progression of breast disease. We generated MCF-7 cell lines expressing DAL-1 constitutively or under the control of an inducible promoter and analyzed the effect of DAL-1 expression on growth. These investigations revealed that the DAL-1 protein suppresses the growth of MCF-7 cells and may do so in part through the induction of apoptosis. In addition, expression of DAL-1 increased attachment of these cells to a variety of extracellular matrices. This is the first evidence that the DAL-1 protein functions at the interface between cell adhesion and apoptosis in controlling cell growth.
AuthorsAubri L Charboneau, Vinita Singh, Tingxi Yu, Irene F Newsham
JournalInternational journal of cancer (Int J Cancer) Vol. 100 Issue 2 Pg. 181-8 (Jul 10 2002) ISSN: 0020-7136 [Print] United States
PMID12115567 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
CopyrightCopyright 2002 Wiley-Liss, Inc.
Chemical References
  • EPB41L3 protein, human
  • Membrane Proteins
  • Microfilament Proteins
  • Tumor Suppressor Proteins
Topics
  • Apoptosis
  • Blotting, Western
  • Breast Neoplasms (genetics, metabolism, pathology)
  • Cell Adhesion
  • Cell Division
  • Electric Impedance
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, Tumor Suppressor
  • Humans
  • Immunoenzyme Techniques
  • In Situ Nick-End Labeling
  • Membrane Proteins (biosynthesis, genetics)
  • Microfilament Proteins
  • Transfection
  • Tumor Cells, Cultured (pathology)
  • Tumor Suppressor Proteins (biosynthesis, genetics)

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