Quantification of Membrane and Membrane-Bound Proteins in Normal and Malignant Breast Cancer Cells Isolated from the Same Patient with Primary Breast Carcinoma

2006 ◽  
Vol 5 (10) ◽  
pp. 2632-2641 ◽  
Author(s):  
Xiquan Liang ◽  
Jenson Zhao ◽  
Mahbod Hajivandi ◽  
Rina Wu ◽  
Janet Tao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Primary Breast Carcinoma ◽  
Malignant Breast ◽  
Membrane Bound

scholarly journals miR-622 is a novel potential biomarker of breast carcinoma and impairs motility of breast cancer cells through targeting NUAK1 kinase

2020 ◽  
Vol 123 (3) ◽  
pp. 426-437
Author(s):  
Francesca Maria Orlandella ◽  
Raffaela Mariarosaria Mariniello ◽  
Peppino Mirabelli ◽  
Anna Elisa De Stefano ◽  
Paola Lucia Chiara Iervolino ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Potential Biomarker

Imatinib-induced changes in gene expression and the metastatic potential of human breast carcinoma cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 1074-1074
Author(s):  
A. Lorico ◽  
F. Anzanello ◽  
G. Rappa
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Carcinoma Cells ◽  
Myelogenous Leukemia ◽  
Breast Carcinoma Cells

1074 Background: Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs). Since its advent for the successful treatment of chronic myelogenous leukemia in 2001, the clinical efficacy of imatinib has been investigated in many other human malignancies, including breast cancer. Based on recent reports that chemotherapy selects more invasive and metastasizing cells, we have hypothesized that exposure of breast cancer cells to imatinib could enhance their malignant behavior. Methods: MA-11 breast carcinoma cells, originating from bone marrow micrometastases, were exposed to imatinib in vitro for seven days. After four days of recovery in drug-free medium, biological properties and gene expression pattern were compared with those of the parental cell line. In a separate set of experiments, the effects of in vivo administration of imatinib to athymic nude (nu/nu) mice carrying MA-11 tumors were investigated. Results: In vitro, imatinib treatment increased the motility and invasiveness of the breast cancer cells, and induced over-expression of drug transporters and of a set of genes associated with aggressive and metastatic behavior (Table). In vivo, nu/nu mice subcutaneously implanted with MA-11 cells and treated with nine daily intraperitoneal doses of 60 mg/Kg imatinib developed with greater frequency distant organ metastases vs. control mice implanted with MA-11 and treated with the vehicle alone. Conclusions: Our data caution against the clinical use of imatinib in breast cancer; imatinib-selected breast cancer cells represent an important tool to investigate the pro-metastatic role of differentially expressed genes. [Table: see text] No significant financial relationships to disclose.

An IgG human monoclonal antibody reactive with a surface membrane antigen expressed on malignant breast cancer cells

1991 ◽  
Vol 2 (2) ◽  
pp. 74-83 ◽  
Author(s):  
Marshall R. Posner ◽  
Hillary S. Elboim ◽  
Marea B. Tumber ◽  
Peter M. Wiest ◽  
Lance M. Tibbetts
Keyword(s):  
Breast Cancer ◽  
Monoclonal Antibody ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Human Monoclonal Antibody ◽  
Surface Membrane ◽  
Malignant Breast

CD24 expression and breast cancer stem cell phenotype

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 11106-11106
Author(s):  
G. Rappa ◽  
F. Anzanello ◽  
A. Lorico
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Carcinoma Cells ◽  
Cell Phenotype ◽  
Cell Cycle Distribution ◽  
Breast Carcinoma Cells ◽  
The Relationship

11106 Background: Several studies suggest the existence of breast cancer-initiating cells (BCIC), responsible for tumor development and progression. Initial reports that only the CD44+CD24−/low subpopulation contains BCIC have been challenged by subsequent studies. We examined the relationship between CD24 and biological properties of breast cancer cells. Methods: MA-11 breast carcinoma cells, originating from bone marrow micrometastases, are CD44+ and have an heterogeneous expression of CD24 (214,000/cell; range 0–1,120,000). We have previously reported that upon in vitro culture as mammospheres under stem cell-like conditions, MA-11 cells acquired increased tumorigenicity and a CD44+CD24−/low phenotype. We have now investigated the relationship between CD24 expression and tumorigenicity in the MA-11 model. Results: Upon passage of MA-11 mammospheres in adherent culture, cells rapidly re-expressed CD 24. The rapid increase in CD24 was consistent with antigen up-regulation, not selection of CD24−/low cells. Exposure of adherent MA-11 cells to imatinib for 72h resulted in a reversible decrease in CD24 from 214,000 to 15,800/cell. CD44+CD24−/low cells, sorted by flow cytometry, generated CD44+CD24high, and CD44+CD24highgenerated CD44+CD24−/low. Immediately after sorting, >90% CD44+CD24−/low cells were in G0/G1. After 24–48 h in culture, cell cycle distribution, growth rate and invasiveness of the sorted cell populations were equivalent. Upon injection and s.c. growth, CD24 expression of CD44+CD24−/low populations and clones increased from 10,000 to 220,000/cell. Similarly, CD44+CD24−/low clones derived from human MCF-7 breast carcinoma cells formed tumors containing >99% CD44+CD24high cells. The average number of CD24 per cell was equivalent for tumors formed upon injection of CD44+CD24−/low, CD44+CD24+, mammosphere-derived cells or parental adherent MA-11 cells. The tumorigenic potentials of sorted CD44+CD24−/low, CD44+CD24−/lowsub-populations and clones in nu/nu mice were equivalent. Conclusions: CD44+CD24−/low breast cancer cells are not associated with increased tumorigenicity; the high CD24 level of mouse xenografts derived from both CD44+CD24−/low and CD44+CD24hi breast cancer cells suggests an important role for CD24 in tumor growth. No significant financial relationships to disclose.

scholarly journals Membrane-bound estrogen receptor alpha initiated signaling is dynamin dependent in breast cancer cells

2018 ◽  
Vol 23 (1) ◽  
Author(s):  
Istvan Marczell ◽  
Petra Balogh ◽  
Gabor Nyiro ◽  
Anna L. Kiss ◽  
Balazs Kovacs ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Alpha ◽  
Receptor Alpha ◽  
Membrane Bound

scholarly journals NFAT promotes carcinoma invasive migration through glypican-6

2011 ◽  
Vol 440 (1) ◽  
pp. 157-166 ◽  
Author(s):  
Gary K. Yiu ◽  
Aura Kaunisto ◽  
Y. Rebecca Chin ◽  
Alex Toker
Keyword(s):  
Breast Cancer ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Regulatory Elements ◽  
Surface Glycoprotein ◽  
Mitogen Activated Protein Kinase ◽  
Proximal Promoter ◽  
Activated T Cells ◽  
Cell Surface Glycoprotein

Invasive migration of carcinoma cells is a prerequisite for the metastatic dissemination of solid tumours. Numerous mechanisms control the ability of cancer cells to acquire a motile and invasive phenotype, and subsequently degrade and invade the basement membrane. Several genes that are up-regulated in breast carcinoma are responsible for mediating the metastatic cascade. Recent studies have revealed that the NFAT (nuclear factor of activated T-cells) is a transcription factor that is highly expressed in aggressive breast cancer cells and tissues, and mediates invasion through transcriptional induction of pro-invasion and migration genes. In the present paper we demonstrate that NFAT promotes breast carcinoma invasion through induction of GPC (glypican) 6, a cell-surface glycoprotein. NFAT transcriptionally regulates GPC6 induction in breast cancer cells and binds to three regulatory elements in the GPC6 proximal promoter. Expression of GPC6 in response to NFAT signalling promotes invasive migration, whereas GPC6 silencing with shRNA (small-hairpin RNA) potently blocks this phenotype. The mechanism by which GPC6 promotes invasive migration involves inhibition of canonical β-catenin and Wnt signalling, and up-regulation of non-canonical Wnt5A signalling leading to the activation of JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase). Thus GPC6 is a novel NFAT target gene in breast cancer cells that promotes invasive migration through Wnt5A signalling.

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