scholarly journals bFGF and aFGF induce membrane ruffling in breast cancer cells but not in normal breast epithelial cells: FGFR-4 involvement

1995 ◽  
Vol 306 (2) ◽  
pp. 609-616 ◽  
Author(s):  
C L Johnston ◽  
H C Cox ◽  
J J Gomm ◽  
R C Coombes
Keyword(s):  
Breast Cancer ◽  
Growth Factors ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Physiological Role ◽  
Normal Breast ◽  
Breast Cancer Cell Lines ◽  
Breast Epithelial Cells ◽  
Membrane Ruffling ◽  
Breast Epithelial

Acidic and basic fibroblast growth factors (aFGF and bFGF) are growth factors which may have a physiological role in the normal breast and in breast cancer. A study of the effects of aFGF and bFGF on a variety of breast cell lines and epithelial cells purified from normal breast organoids showed that whereas normal breast cells did not exhibit membrane ruffling in response to either of these growth factors, some breast cancer cell lines did. This difference was not due to lack of receptor since all the cell lines tested were mitogenically stimulated by bFGF. Dominant negative mutations of FGF receptor 3 (FGFR-3) and the small GTP-binding protein p21rac inhibited membrane ruffling, showing that receptor dimerization and phosphorylation and p21rac activation are prerequisites for membrane ruffling in response to aFGF and bFGF. Transient transfection of individual FGFRs into cos-7 cells showed that FGFR-1, FGFR-2 and FGFR-3 could not mediate a membrane ruffling response whereas FGFR-4 could. These studies elucidate one signalling mechanism of FGF and point to differences in the response of normal and cancer breast epithelial cells which may be important in cell motility.

scholarly journals Expression of estrogen receptor β isoforms in normal breast epithelial cells and breast cancer: regulation by methylation

Oncogene ◽  
2003 ◽  
Vol 22 (48) ◽  
pp. 7600-7606 ◽  
Author(s):  
Chunyan Zhao ◽  
Eric W-F Lam ◽  
Andrew Sunters ◽  
Eva Enmark ◽  
Manuela Tamburo De Bella ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Normal Breast ◽  
Estrogen Receptor Β ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Normal Breast Epithelial Cells

scholarly journals Bringing androgens up a NOTCH in breast cancer

2014 ◽  
Vol 21 (4) ◽  
pp. T183-T202 ◽  
Author(s):  
Gerard A Tarulli ◽  
Lisa M Butler ◽  
Wayne D Tilley ◽  
Theresa E Hickey
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Normal Breast ◽  
Notch Signalling ◽  
Breast Development ◽  
Breast Epithelium ◽  
Breast Epithelial Cells ◽  
Androgen Action ◽  
Breast Epithelial

While it has been known for decades that androgen hormones influence normal breast development and breast carcinogenesis, the underlying mechanisms have only been recently elucidated. To date, most studies have focused on androgen action in breast cancer cell lines, yet these studies represent artificial systems that often do not faithfully replicate/recapitulate the cellular, molecular and hormonal environments of breast tumoursin vivo. It is critical to have a better understanding of how androgens act in the normal mammary gland as well as inin vivosystems that maintain a relevant tumour microenvironment to gain insights into the role of androgens in the modulation of breast cancer development. This in turn will facilitate application of androgen-modulation therapy in breast cancer. This is particularly relevant as current clinical trials focus on inhibiting androgen action as breast cancer therapy but, depending on the steroid receptor profile of the tumour, certain individuals may be better served by selectively stimulating androgen action. Androgen receptor (AR) protein is primarily expressed by the hormone-sensing compartment of normal breast epithelium, commonly referred to as oestrogen receptor alpha (ERa (ESR1))-positive breast epithelial cells, which also express progesterone receptors (PRs) and prolactin receptors and exert powerful developmental influences on adjacent breast epithelial cells. Recent lineage-tracing studies, particularly those focussed on NOTCH signalling, and genetic analysis of cancer risk in the normal breast highlight how signalling via the hormone-sensing compartment can influence normal breast development and breast cancer susceptibility. This provides an impetus to focus on the relationship between androgens, AR and NOTCH signalling and the crosstalk between ERa and PR signalling in the hormone-sensing component of breast epithelium in order to unravel the mechanisms behind the ability of androgens to modulate breast cancer initiation and growth.

Human chorionic gonadotropin and a 15 amino acid hCG fragment of the hormone induce downregulation of the cytokine IL-8 receptor in normal breast epithelial cells

2011 ◽  
Vol 6 (3) ◽  
Author(s):  
Samuel M.R. Noronha ◽  
Silvana A.A. Correa-Noronha ◽  
Irma H. Russo ◽  
Ricardo López de Cicco ◽  
Julia Santucci-Pereira ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Amino Acid ◽  
Epithelial Cells ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Normal Breast ◽  
Breast Cancer Cell Lines ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Normal Breast Epithelial Cells

AbstractCytokine receptors are associated with tumor cell growth by increasing proliferation, metastasis and regulating self-renewal of cancer stem cells (SCs). There is a strong association between cytokine IL-8 receptor (CXCR1) over-expression and cells displaying SC characteristics. Human chorionic gonadotropin (hCG) causes differentiation, inhibition of cell proliferation and increased apoptosis of the breast epithelium. hCG receptor (LHCGR) expression in breast tumors and in breast cancer cell lines is undetectable or low. In this study, our objective was to assess and compare the effects of hCG and a 15 amino acid hCG fragment of the hormone on mRNA expression of CXCR1 and LHCGR on normal breast epithelial cells (MCF-10F) by real time RT-PCR after treatment with hCG or a hCG fragment for 15 days. Cell proliferation was also measured. hCG and the hCG fragment decreased cell proliferation in both groups. The compounds upregulated LHCGR expression and downregulated CXCR1 expression. It is possible to postulate that an increase of LHCGR mRNA seems to respond to the decrease of CXCR1 expression. These genes probably act synergistically to reduce the amount of cancer SCs in the mammary gland. Thereby, the use of hCG or the hCG fragment as a therapeutic or preventive tool should be considered.

Cytochemical and biochemical evidence of cathepsin B in malignant, transformed and normal breast epithelial cells

1987 ◽  
Vol 87 (1) ◽  
pp. 145-154
Author(s):  
E. Krepela ◽  
J. Bartek ◽  
D. Skalkova ◽  
J. Vicar ◽  
D. Rasnick ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cathepsin B ◽  
Proteinase Inhibitors ◽  
Cysteine Proteinase ◽  
Normal Breast ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Normal Breast Epithelial Cells

Human breast cancer cell lines, as well as transformed mammary epithelial cells (HBL-100) and growth-stimulated normal breast epithelial cells showed positive cytochemical reaction with the proteinase substrate 2-(N-benzyloxycarbonyl-L-arginyl-L-arginylamido)-4-methoxynapht halene, in the presence of 5-nitrosalicylaldehyde. The reaction product, small fluorescent granules, was distributed throughout the cytoplasm, in the perinuclear zone, in some cytoplasmic projections, and at the cell surface. Using a panel of various proteinase inhibitors, we found that the formation of the reaction product was an enzymic function of a cysteine proteinase. Using the substrate 7-(N-benzyloxycarbonyl-L-arginyl-L-arginylamido)-4-methylcoumarin, we evaluated some biochemical properties of the cysteine proteinase, including pH-activity profile, pH stability, apparent relative molecular mass and sensitivity toward various proteinase inhibitors. We found that the proteinase from the studied breast epithelial cells exhibited characteristics of a mature form of cathepsin B. Taken together, the cytochemical and biochemical data provide evidence that human breast epithelial cells of cancer origin, as well as in the transformed or growth-stimulated state express active cathepsin B and compartmentalize it into specific subcellular sites.

Normal Breast Epithelial Cells Induce Apoptosis of MCF-7 Breast Cancer Cells through a p53-Mediated Pathway

2000 ◽  
Vol 3 (6) ◽  
pp. 338-344 ◽  
Author(s):  
Robert-Alain Toillon ◽  
Eric Adriaenssens ◽  
Danièle Wouters ◽  
Severine Lottin ◽  
Bénoni Boilly ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Normal Breast ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Normal Breast Epithelial Cells ◽  
Mcf 7

Antigenic heterogeneity of breast cell lines detected by monoclonal antibodies and its relationship with the cell cycle

1985 ◽  
Vol 73 (1) ◽  
pp. 321-333
Author(s):  
P.A. Edwards ◽  
R.A. Skilton ◽  
A.W. Payne ◽  
M.G. Ormerod
Keyword(s):  
Cell Cycle ◽  
Monoclonal Antibodies ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Antigen Expression ◽  
Normal Breast ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Normal Breast Epithelial Cells ◽  
Antigenic Heterogeneity

Established cell lines were stained by immunofluorescence with four monoclonal antibodies to study the phenomenon of antigenic heterogeneity and its possible relation to the cell cycle. Five cell lines thought to be of breast origin, MCF-7, ZR-75-1, T47D, MDA-MB-231 and HBL-100, were stained with three monoclonal antibodies (LICR-LON-M8, LICR-LON-M18, LICR-LON-M24) that each stain a distinct subset of normal breast epithelial cells, i.e. demonstrate antigenic heterogeneity in normal breast epithelial cells. Contrasting monoclonal antibodies LICR-LON-FIB75 and LICR-LON-FIB86 to homogeneously expressed antigens were also used. For the antibodies demonstrating heterogeneity distinct positive and negative fractions were not seen by flow cytometry; the intensity of fluorescence varied continuously from background to a hundred times stronger than background. Fluorescent DNA staining showed no obvious relation between antigen expression and the cell cycle. The essentially constant proportion of cells of a given antigenic phenotype in the various phases suggests that these antibodies do not distinguish a phenotype associated with a distinct proliferating population of cells.

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