Cytokeratins are exposed on the outer surface of established human mammary carcinoma cells

1991 ◽  
Vol 99 (3) ◽  
pp. 595-607 ◽  
Author(s):  
E. Godfroid ◽  
M. Geuskens ◽  
T. Dupressoir ◽  
I. Parent ◽  
C. Szpirer
Keyword(s):  
Outer Surface ◽  
Mammary Carcinoma ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Carcinoma Cells ◽  
Human Mammary Carcinoma ◽  
Two Dimensional Gel Electrophoresis ◽  
Human Mammary Epithelial ◽  
Mammary Carcinoma Cells ◽  
Normal Human

Normal human mammary epithelial cells and established tumour cells of the same origin express three to eight cytokeratins, which are distributed throughout the cytoplasm in the form of intermediate filaments. The combined use of the iodogen and the two-dimensional gel electrophoresis methods has allowed us to demonstrate the presence of cytokeratins 8, 18 and 19 on the outer surface of established human mammary carcinoma cells, in particular MCF-7 cells, while they were absent from the surface of normal mammary cells in primary culture. By ultrastructural immunocytochemistry, these cytokeratins were localized on blebs formed by the cell surface. Cytokeratins 8, 18 and 19 were also detected in the culture medium of mammary carcinoma cells.

Effect of the extracellular matrix on plasminogen activator isozyme activities of human mammary epithelial cells in culture

1983 ◽  
Vol 3 (6) ◽  
pp. 982-990
Author(s):  
N S Yang ◽  
C Park ◽  
C Longley ◽  
P Furmanski
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Plasminogen Activator ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Collagen Gels ◽  
Human Mammary Epithelial Cells ◽  
Human Mammary Epithelial ◽  
Normal Human ◽  
Mcf 7

Multiple molecular forms of plasminogen activator were detected in normal human mammary epithelial cells in culture. Cells derived from (normal) breast mammoplasty specimens and grown on the surface of collagen gels exhibited three major classes of plasminogen activator isozymes (Mr = 100,000 [100K], 75,000 [75K], and 55,000 [55K]). The activity of the 100K and 75K isozymes was greatly reduced when the cells were grown on conventional tissue-culture-grade plastic surfaces. MCF-7, a human mammary carcinoma cell line, exhibited predominantly or exclusively the 55K isozyme, irrespective of the cell growth substratum. The activity of the 55K isozyme was more than twofold higher for MCF-7 cells grown on collagen gels than for cells grown on plastic. Progesterone, diethylstilbestrol, and estrogen stimulated the activity of the 55K isozyme of MCF-7 cells, but only when the cells were grown on a plastic surface. The plasminogen activator activities of the normal human mammary epithelial cells were not stimulated by these hormones, irrespective of the growth substratum. These results show that the expression of plasminogen activator isozymes by human mammary epithelial cells is subject to modulation by the extracellular matrix. Normal and malignant cells may differ in their responsiveness to these effects.

Signal Transducer and Activator of Transcription (STAT)-5A and STAT5B Differentially Regulate Human Mammary Carcinoma Cell Behavior

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 43-55 ◽  
Author(s):  
Jian-Zhong Tang ◽  
Ze-Hua Zuo ◽  
Xiang-Jun Kong ◽  
Michael Steiner ◽  
Zhinan Yin ◽  
...  
Keyword(s):  
Cell Motility ◽  
Mammary Carcinoma ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Signal Transducer ◽  
Human Mammary Carcinoma ◽  
Anchorage Independent Growth ◽  
Human Mammary Carcinoma Cell ◽  
Mammary Carcinoma Cells ◽  
Interfering Rna

Abstract Increased activation of signal transducer and activator of transcription (STAT)-5 has been reported in various malignancies including mammary carcinoma. However, it is only recently that potentially distinct roles of STAT5A and STAT5B in neoplasia have begun to emerge. Herein we systematically delineate the functions of STAT5A and STAT5B in human mammary carcinoma cell lines MCF-7 and T47D. Forced expression of constitutively active (CA) STAT5A enhanced both survival and anchorage-independent growth of human mammary carcinoma cells but concordantly suppressed cell motility as revealed in colony scattering, cell migration, and invasion assays. In contrast, forced expression of CA STAT5B exhibited lower potency than CA STAT5A in enhancing survival and anchorage-independent growth of mammary carcinoma cells and exerted no effects on cell motility. Differential expression of genes that regulate cellular survival and motility was concomitantly observed on forced expression of CA STAT5A or CA STAT5B. Small interfering RNA-mediated depletion of STAT5A significantly impaired anchorage-independent growth of human mammary carcinoma cells, whereas a smaller reduction was observed upon small interfering RNA-mediated depletion of STAT5B. Depletion of endogenous STAT5A also significantly enhanced cell motility, whereas depletion of endogenous STAT5B exhibited no effect. Xenograft studies provided data concordant with the in vitro effects of the two STAT5 isoforms. We therefore demonstrate that STAT5A and STAT5B differentially regulate behavior of human mammary carcinoma cells.

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