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International Journal of Cancer
Article . 2002 . Peer-reviewed
License: Wiley Online Library User Agreement
Data sources: Crossref
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Suppression of growth and increased cellular attachment after expression of DAL‐1 in MCF‐7 breast cancer cells

Authors: Aubri L, Charboneau; Vinita, Singh; Tingxi, Yu; Irene F, Newsham;

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

Abstract

AbstractThe 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. © 2002 Wiley‐Liss, Inc.

Related Organizations
Keywords

Tumor Suppressor Proteins, Blotting, Western, Microfilament Proteins, Membrane Proteins, Apoptosis, Breast Neoplasms, Transfection, Gene Expression Regulation, Neoplastic, Immunoenzyme Techniques, Cell Adhesion, Electric Impedance, In Situ Nick-End Labeling, Tumor Cells, Cultured, Humans, Female, Genes, Tumor Suppressor, Cell Division

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    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
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    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
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    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
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    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
59
Average
Top 10%
Top 10%
bronze