scholarly journals Differential Expression of Human Tissue Factor in Normal Mammary Epithelial Cells and in Carcinomas

1995 ◽  
Vol 1 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Zehan Chen ◽  
Ruth Sager
Keyword(s):  
Epithelial Cells ◽  
Tissue Factor ◽  
Differential Expression ◽  
Human Tissue ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Normal Mammary Epithelial

The role of laminin-5 and its receptors in mammary epithelial cell branching morphogenesis

1997 ◽  
Vol 110 (1) ◽  
pp. 55-63 ◽  
Author(s):  
S. Stahl ◽  
S. Weitzman ◽  
J.C. Jones
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Branching Morphogenesis ◽  
Mammary Epithelial ◽  
Breast Epithelial Cell ◽  
Epithelial Tissue ◽  
Laminin 5 ◽  
Normal Mammary Epithelial

In vivo, normal mammary epithelial cells utilize hemidesmosome attachment devices to adhere to stroma. However, analyses of a potential role for hemidesmosomes and their components in mammary epithelial tissue morphogenesis have never been attempted. MCF-10A cells are a spontaneously immortalized line derived from mammary epithelium and possess a number of characteristics of normal mammary epithelial cells including expression of hemidesmosomal associated proteins such as the two bullous pemphigoid antigens, alpha 6 beta 4 integrin and its ligand laminin-5. More importantly, MCF-10A cells readily assemble mature hemidesmosomes when plated onto uncoated substrates. When maintained on matrigel, like their normal breast epithelial cell counterparts, MCF-10A cells undergo a branching morphogenesis and assemble hemidesmosomes at sites of cell-matrigel interaction. Function blocking antibodies specific for human laminin-5 and the alpha subunits of its two known receptors (alpha 3 beta 1 and alpha 6 beta 4 integrin) not only inhibit hemidesmosome assembly by MCF-10A cells but also impede branching morphogenesis induced by matrigel. Our results imply that the hemidesmosome, in particular those subunits comprising its laminin-5/integrin ‘backbone’, play an important role in morphogenetic events. We discuss these results in light of recent evidence that hemidesmosomes are sites involved in signal transduction.

scholarly journals Plasticity of patient-matched normal mammary epithelial cells is dependent on autologous adipose-derived stem cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Annika Kengelbach-Weigand ◽  
Kereshmeh Tasbihi ◽  
Pamela L. Strissel ◽  
Rafael Schmid ◽  
Jasmin Monteiro Marques ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Adipose Derived Stem Cells ◽  
Normal Mammary Epithelial

Physical Connections between Feeder Cells and Recipient Normal Mammary Epithelial Cells

1998 ◽  
Vol 243 (1) ◽  
pp. 76-86 ◽  
Author(s):  
Ursula K. Ehmann ◽  
Mary Ann Stevenson ◽  
Stuart K. Calderwood ◽  
James T. DeVries
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Feeder Cells ◽  
Normal Mammary Epithelial

scholarly journals Influence of fatty acid diets on gene expression in rat mammary epithelial cells

2009 ◽  
Vol 38 (1) ◽  
pp. 80-88 ◽  
Author(s):  
M. Medvedovic ◽  
R. Gear ◽  
J. M. Freudenberg ◽  
J. Schneider ◽  
R. Bornschein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Epithelial Cells ◽  
Differential Expression ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Differentially Expressed ◽  
Cell Cycle Genes

Background: This study examines the impact of dietary fatty acids on regulation of gene expression in mammary epithelial cells before and during puberty. Methods: Diets primarily consisted of n-9 monounsaturated fatty acids (olive oil), n-6 polyunsaturated fatty acids (safflower), saturated acids (butter), and the reference AIN-93G diet (soy oil). The dietary regimen mimics the repetitive nature of fatty acid exposure in Western diets. Diet-induced changes in gene expression were examined in laser capture microdissected mammary ductal epithelial cells at day of weaning and end of puberty. PCNA immunohistochemistry analysis compared proliferation rates between diets. Results: Genes differentially expressed between each test diets and the reference diet were significantly enriched by cell cycle genes. Some of these genes were involved in activation of the cell cycle pathway or the G2/M check point pathway. Although there were some differences in the level of differential expression, all diets showed qualitatively the same pattern of differential expression compared to the reference diet. Cluster analysis identified an expanded set of cell cycle as well as immunity and sterol metabolism related clusters of differentially expressed genes. Conclusion: Fatty acid-enriched diets significantly upregulated proliferation above normal physiological levels during puberty. Higher cellular proliferation during puberty caused by enriched fatty acid diets poses a potential increase risk of mammary cancer in later life. The human homologs of 27 of 62 cell cycle rat genes are included in a human breast cancer cluster of 45 cell cycle genes, further emphasizing the importance of our findings in the rat model.

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