scholarly journals The a3 isoform of subunit a of the vacuolar ATPase localizes to the plasma membrane of invasive breast tumor cells and is overexpressed in human breast cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (29) ◽  
pp. 46142-46157 ◽  
Author(s):  
Kristina Cotter ◽  
Rachel Liberman ◽  
GeHong Sun-Wada ◽  
Yoh Wada ◽  
Dennis Sgroi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Plasma Membrane ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Vacuolar Atpase ◽  
Human Breast ◽  
Subunit A ◽  
Breast Tumor Cells ◽  
Invasive Breast Tumor

Characterization of human breast cancer tissues by infrared imaging

The Analyst ◽  
2016 ◽  
Vol 141 (2) ◽  
pp. 606-619 ◽  
Author(s):  
M. Verdonck ◽  
A. Denayer ◽  
B. Delvaux ◽  
S. Garaud ◽  
R. De Wind ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Infrared Imaging ◽  
Human Breast ◽  
Automated Identification ◽  
Breast Tumor Cells ◽  
Cancer Tissues

FTIR imaging allows automated identification and quantification of breast tumor cells as well as investigating tumor-related stroma alterations.

scholarly journals Productive Infection of Human Breast Cancer Cell Lines with Human Cytomegalovirus (HCMV)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 641
Author(s):  
Kaitlin M. Branch ◽  
Erica C. Garcia ◽  
Yin Maggie Chen ◽  
Matthew McGregor ◽  
Mikayla Min ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Tumor Cells

Breast cancer is the leading cause of cancer deaths among women worldwide. There are many known risk factors for breast cancer, but the role of infectious disease remains unclear. Human cytomegalovirus (HCMV) is a widespread herpesvirus that usually causes little disease. Because HCMV has been detected in breast tumor biopsy samples and is frequently transmitted via human breast milk, we investigated HCMV replication in breast tumor cells. Four human breast cancer cell lines with different expression profiles for the key diagnostic markers of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were infected with a bacterial artificial chromosome-derived HCMV clinical strain TB40/E tagged with green fluorescent protein (GFP). Fluorescence microscopy confirmed that all four breast cancer cell lines supported virus entry. RNA was isolated from infected cells and the expression of immediate early (UL123), early (UL54), and late (UL111A) genes was confirmed using PCR. Viral proteins were detected by immunoblotting, and viral progeny were produced during the infection of breast tumor cells, as evidenced by subsequent infection of fibroblasts with culture supernatants. These results demonstrate that breast tumor cells support productive HCMV infection and could indicate that HCMV replication may play a role in breast cancer progression.

scholarly journals Interactions between estrogen and insulin-like growth factor signaling pathways in human breast tumor cells.

2003 ◽  
pp. 331-345 ◽  
Author(s):  
I H L Hamelers ◽  
P H Steenbergh
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Signaling Pathways ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Synergistic Effects ◽  
Human Breast ◽  
Breast Tumor Cells ◽  
Igf I

Estrogens and insulin-like growth factors (IGFs) act as mitogens promoting cell proliferation in normal breast tissue as well as in breast carcinomas. Both hormones have been shown to play a role in the development of breast cancer and were found to activate multiple signaling pathways leading to proliferation of human breast cancer cell lines in vitro. Originally, it was considered that these agents manifest their mitogenic actions through separate pathways, but a growing body of evidence suggests that the IGF- and estrogen-mediated signaling pathways are intertwined. 17beta-Estradiol (E2) has been shown to enhance IGF signaling at multiple levels. E2 treatment of breast cancer cells alters expression of nearly all of the IGF family members including IGF-I, IGF-II, IGF-binding proteins, IGF type I receptor (IGF-RI), and insulin receptor substrate 1. The ligand-bound estrogen receptor has been reported to bind to and to activate the IGF-RI directly. Vice versa, IGF signaling has been reported to enhance estrogen receptor activation in human breast cancer cells by inducing phosphorylation of the estrogen receptor. Finally, several groups have described synergistic effects of the combination of E2 and IGF-I on S phase entry in breast tumor cell lines. Here, we review recent, often contradictory, reports describing the effects of E2 and IGFs on the proliferation of breast tumor cells, with special emphasis on the synergistic effects of the two hormones.

Vacuolar H+-ATPase in human breast cancer cells with distinct metastatic potential: distribution and functional activity

2004 ◽  
Vol 286 (6) ◽  
pp. C1443-C1452 ◽  
Author(s):  
Souad R. Sennoune ◽  
Karina Bakunts ◽  
Gloria M. Martínez ◽  
Jenny L. Chua-Tuan ◽  
Yamina Kebir ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Plasma Membrane ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cytosolic Ph ◽  
Metastatic Cells

Tumor cells thrive in a hypoxic microenvironment with an acidic extracellular pH. To survive in this harsh environment, tumor cells must exhibit a dynamic cytosolic pH regulatory system. We hypothesize that vacuolar H+-ATPases (V-ATPases) that normally reside in acidic organelles are also located at the cell surface, thus regulating cytosolic pH and exacerbating the migratory ability of metastatic cells. Immunocytochemical data revealed for the first time that V-ATPase is located at the plasma membrane of human breast cancer cells: prominent in the highly metastatic and inconspicuous in the lowly metastatic cells. The V-ATPase activities in isolated plasma membranes were greater in highly than in lowly metastatic cells. The proton fluxes via V-ATPase evaluated by fluorescence spectroscopy in living cells were greater in highly than in lowly metastatic cells. Interestingly, lowly metastatic cells preferentially used the ubiquitous Na+/H+exchanger and HCO3−-based H+-transporting mechanisms, whereas highly metastatic cells used plasma membrane V-ATPases. The highly metastatic cells were more invasive and migratory than the lowly metastatic cells. V-ATPase inhibitors decreased the invasion and migration in the highly metastatic cells. Altogether, these data indicate that V-ATPases located at the plasma membrane are involved in the acquisition of a more metastatic phenotype.

On the Cytotoxicity of Chiral Ruthenium Complexes Containing Sulfur Amino Acids Against Breast Tumor Cells (MDA-231 and MCF-7)

2020 ◽  
Vol 20 ◽  
Author(s):  
Celisnolia M. Leite ◽  
João Honorato de Araujo-Neto ◽  
Rodrigo S. Corrêa ◽  
Legna Colina-Vegas ◽  
Diego Martínez-Otero ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Amino Acids ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Ruthenium Complexes ◽  
Sulfur Amino Acids ◽  
Human Breast ◽  
Mcf 7

Background: Breast cancer is one of the most common types among women. Its incidence progressively increases with age, especially after age 50. Platinum compounds are not efficient in the treatment of breast cancer, highlighting the use of other metals for the development of new chemotherapeutic agents. Objective: This paper aims to obtain three new ruthenium compounds that incorporate sulfur amino acids in their structures and to investigate their cytotoxic activity in breast tumor cell lines. Methods: Complexes with general formula [Ru(AA)(dppb)(bipy)] (complexes 1 and 2) or [Ru(AA)(dppb)(bipy)]PF6 (complex 3), where AA = L-cysteinate (1), D-penicillaminate (2), and L-deoxyalliinate (3), dppb = 1,4- bis(diphenylphosphino)butane and 2,2´-bipyridine, were obtained from the cis-[RuCl2(dppb)(bipy)] precursor. The cytotoxicity of the complexes on MDA-MB-231 (triple negative human breast cancer); MCF-7 (double positive human breast cancer) and V79 (hamster lung fibroblast) were performed by the MTT (4,5-dimethylthiazol-2-yl-2,5- diphenyltetrazolium bromide) method. The control agent was the cisplatin, which is a commercially available drug for cancer treatment. Results: In complexes (1) and (2), the ligands are coordinated to the metal center by nitrogen and sulfur atoms, while in complex (3) coordination is through the oxygen and nitrogen atoms. These suggestions are based on the infrared and 31P1H NMR data. For complexes (1) and (2), their X-ray structures were determined confirming this suggestion. The three complexes are stable in a mixture of DMSO (80 %) and biological medium (20 %) for at least 48 h and presented cytotoxicity against the MDA-MB-231 and MCF-7 tumor cells with reasonable selectivity indexes. Conclusion: Our work demonstrated that ruthenium complexes containing sulfur amino acids, bipyridines and bisphosphines showed cytotoxicity against the MDA-MB-231 and MCF-7 cancer cell lines, in vitro, and that they interact weakly with the DNA (Deoxyribonucleic Acid) and the HSA (Human Serum Albumin) biomolecules.

scholarly journals A Method to Monitor mRNA Levels in Human Breast Tumor Cells Obtained by Fine-needle Aspiration

1997 ◽  
Vol 6 (6) ◽  
pp. 353-360 ◽  
Author(s):  
Majella S. de Lange ◽  
Bert Top ◽  
Caro Lambrechts ◽  
Riks A. Maas ◽  
Hans L. Peterse ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Fine Needle Aspiration ◽  
Breast Tumor ◽  
Needle Aspiration ◽  
Mrna Levels ◽  
Human Breast ◽  
Human Breast Tumor ◽  
Breast Tumor Cells ◽  
Fine Needle

Induction of Apoptosis by Hybrid Liposomes without Antitumor Drugs toward Human Breast Tumor Cells

2003 ◽  
Vol 36 (9) ◽  
pp. 1127-1129 ◽  
Author(s):  
Hideaki Nagami ◽  
Keiichi Yamamoto ◽  
Hideaki Ichihara ◽  
Yoko Matsumoto ◽  
Ryuichi Ueoka
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Antitumor Drugs ◽  
Human Breast ◽  
Human Breast Tumor ◽  
Breast Tumor Cells ◽  
Induction Of Apoptosis

scholarly journals Biochemical and Anti-Triple Negative Metastatic Breast Tumor Cell Properties of Psammaplins

Marine Drugs ◽  
2018 ◽  
Vol 16 (11) ◽  
pp. 442 ◽  
Author(s):  
Yu-Dong Zhou ◽  
Jun Li ◽  
Lin Du ◽  
Fakhri Mahdi ◽  
Thuy Le ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Triple Negative ◽  
Hdac Inhibitors ◽  
Metastatic Breast ◽  
Dependent Manner ◽  
Breast Tumor Cells ◽  
Metastatic Breast Tumor

Breast tumors reprogram their cellular metabolism, nutrient uptake, and utilization-associated biochemical processes. These processes become further transformed as genetically predisposed metastatic breast tumor cells colonize specific organs. Breast tumor cells often metastasize to the brain, bone, lung and liver. Massagué and colleagues isolated organotropic subclones and established organ-specific gene signatures associated with lung-, bone-, and brain-specific metastatic triple-negative breast cancer (TNBC) MDA-MB-231 cells. Using these genetically characterized metastatic subclones specific to lung (LM4175), bone (BoM1833), and brain (BrM-2a), we evaluated marine natural products for the ability to differentially suppress metastatic breast cancer cells in a target organ-dependent manner. Psammaplin-based histone deacetylase (HDAC) inhibitors were found to differentially inhibit HDAC activity, induce activation of hypoxia-inducible factor-1 (HIF-1), and disrupt organotropic metastatic TNBC subclone growth. Further, psammaplins distinctly suppressed the outgrowth of BoM1833 tumor spheroids in 3D-culture systems. Similar results were observed with the prototypical HDAC inhibitor trichostatin A (TSA). These organotropic tumor cell-based studies suggest the potential application of HDAC inhibitors that may yield new directions for anti-metastatic breast tumor research and drug discovery.

Connexin26 Regulates the Expression of Angiogenesis-Related Genes in Human Breast Tumor Cells by Both GJIC-Dependent and -Independent Mechanisms

2003 ◽  
Vol 10 (4) ◽  
pp. 387-393 ◽  
Author(s):  
Hong Qin ◽  
Qing Shao ◽  
Tamsin Thomas ◽  
Jessica Kalra ◽  
Moulay Alaoui-Jamali ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Human Breast ◽  
Human Breast Tumor ◽  
Breast Tumor Cells
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