Expression Levels and Clinical-Pathological Correlations of HER2/neu in Primary and Metastatic Human Breast Cancer

2004 ◽  
Vol 1028 (1) ◽  
pp. 463-472 ◽  
Author(s):  
R. STEFANO
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Expression Levels

scholarly journals High expression levels of egfl7 correlate with low endothelial cell activation in peritumoral vessels of human breast cancer

2016 ◽  
Vol 12 (2) ◽  
pp. 1422-1428 ◽  
Author(s):  
Diane Pannier ◽  
Géraldine Philippin-Lauridant ◽  
Marie-Christine Baranzelli ◽  
Delphine Bertin ◽  
Emilie Bogart ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endothelial Cell ◽  
Human Breast Cancer ◽  
Cell Activation ◽  
High Expression ◽  
Human Breast ◽  
Endothelial Cell Activation ◽  
Expression Levels ◽  
Peritumoral Vessels

E1AF Expression Levels are not Associated with Prognosis in Human Breast Cancer

2003 ◽  
Vol 79 (1) ◽  
pp. 129-131 ◽  
Author(s):  
Paul N. Span ◽  
Peggy Manders ◽  
Joop J.T.M. Heuvel ◽  
Louk V.A.M. Beex ◽  
C.G.J. (Fred) Sweep
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Expression Levels

scholarly journals Actinomycin V Inhibits Migration and Invasion via Suppressing Snail/Slug-Mediated Epithelial-Mesenchymal Transition Progression in Human Breast Cancer MDA-MB-231 Cells In Vitro

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 305 ◽  
Author(s):  
Shiqi Lin ◽  
Caiyun Zhang ◽  
Fangyuan Liu ◽  
Jiahui Ma ◽  
Fujuan Jia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Actinomycin D ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Human Breast ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
E Cadherin

Actinomycin V, an analog of actinomycin D produced by the marine-derived actinomycete Streptomyces sp., possessing a 4-ketoproline instead of a 4-proline in actinomycin D. In this study, the involvement of snail/slug-mediated epithelial-mesenchymal transition (EMT) in the anti-migration and -invasion actions of actinomycin V was investigated in human breast cancer MDA-MB-231 cells in vitro. Cell proliferation effect was evaluated by 3-(4,5-Dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay. Wound-healing and Transwell assay were performed to investigate the anti-migration and -invasion effects of actinomycin V. Western blotting was used to detect the expression levels of E-cadherin, N-cadherin, vimentin, snail, slug, zinc finger E-box binding homeobox 1 (ZEB1), and twist proteins and the mRNA levels were detected by rt-PCR. Actinomycin V showed stronger cytotoxic activity than that of actinomycin D. Actinomycin V up-regulated both of the protein and mRNA expression levels of E-cadherin and down-regulated that of N-cadherin and vimentin in the same cells. In this connection, actinomycin V decreased the snail and slug protein expression, and consequently inhibited cells EMT procession. Our results suggest that actinomycin V inhibits EMT-mediated migration and invasion via decreasing snail and slug expression, which exhibits therapeutic potential for the treatment of breast cancer and further toxicity investigation in vivo is needed.

scholarly journals BCL-XL blockage in TNBC models confers vulnerability to inhibition of specific cell cycle regulators

2021 ◽  
Author(s):  
Olivier Castellanet ◽  
Fahmida Ahmad ◽  
Yaron Vinik ◽  
Gordon B Mills ◽  
Bianca H Habermann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Human Breast Cancer ◽  
Specific Cell ◽  
Cell Cycle Regulators ◽  
Human Breast ◽  
Primary Resistance ◽  
Western Blots ◽  
Expression Levels ◽  
Cellular Localisation

Cell cycle regulators are frequently altered in Triple-Negative Breast Cancer (TNBC). Emerging agents targeting these signals offer the possibility to design new combinatorial therapies. However, preclinical models that recapitulate TNBC primary resistance and heterogeneity are essential to evaluate the potency of these combined treatments. Methods: Bioinformatic processing of human breast cancer datasets was used to analyse correlations between expression levels of cell cycle regulators and patient survival outcome. The MMTV-R26Met mouse model of TNBC resistance and heterogeneity was employed to analyse expression and targeting vulnerability of cell cycle regulators in the presence of BCL-XL blockage. Robustness of outcomes and selectivity was further explored using a panel of human breast cancer cells. Alterations of protein expression, phosphorylation, and/or cellular localisation were analysed by western blots, reverse phase protein array, and immunocytochemistry. Bioinformatics was performed to highlight drug's mechanisms of action. Results: We report that high expression levels of BCL-XL and specific cell cycle regulators correlate with poor survival outcomes of TNBC patients. Blockage of BCL-XL confers vulnerability to drugs targeting CDK1/2/4, but not FOXM1, CDK4/6, Aurora A and Aurora B, to all MMTV-R26Met and human TNBC cell lines tested. Mechanistically, we show that, co-targeting of BCL-XL and CDK1/2/4 synergistically inhibited cell growth by combinatorial depletion of survival and RTK/AKT signals, and concomitantly restoring FOXO3a tumour suppression actions. This was accompanied by an accumulation of DNA damage and consequently apoptosis. Conclusions: Our studies illustrate the possibility to exploit the vulnerability of TNBC cells to CDK1/2/4 inhibition by targeting BCL-XL. Moreover, they underline that specificity matters in targeting cell cycle regulators for combinatorial anticancer therapies.

scholarly journals Reduced expression levels of let-7c in human breast cancer patients

2015 ◽  
Vol 9 (3) ◽  
pp. 1207-1212 ◽  
Author(s):  
XIN-XIN LI ◽  
SHU-YAN GAO ◽  
PING-YU WANG ◽  
XUE ZHOU ◽  
YOU-JIE LI ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Human Breast Cancer ◽  
Breast Cancer Patients ◽  
Human Breast ◽  
Expression Levels

scholarly journals The phospholipase D inhibitor FIPI potently blocks EGF-induced calcium signaling in human breast cancer cells

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Helena M. Stricker ◽  
Nadine Rommerswinkel ◽  
Silvia Keil ◽  
Sandina A. Gnoth ◽  
Bernd Niggemann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Calcium Signaling ◽  
Cancer Cells ◽  
Phospholipase D ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Calcium Release ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Expression Levels

Abstract Background Phosphotyrosine kinase (PTK)-mediated phospholipase C-γ1 (PLC-γ1) signaling plays a crucial role in the release of the universal second messenger calcium from intracellular stores, which is mandatory for several cellular processes, including cell migration. However, PLC-γ1 could also be activated in a PTK-independent manner by phospholipase D (PLD)-derived phosphatidic acid (PA). Because both higher PLD expression levels and PLD activity have also been associated with breast cancer cell invasion and migration, we wondered whether there might be a link between PLD and PLC-γ1, which was investigated in this study. Materials MDA-MB-468-NEO (EGFR positive) and MDA-MB-468-HER2 (EGFR and HER2 positive) human breast cancer cells were used in this study. The migratory behavior of the cells in the presence of epidermal growth factor (EGF) and the PLD inhibitor 5-fluoro-2-indolyl-des-chlorohalopemide (FIPI) was analyzed using the 3D collagen matrix migration assay. Changes in cytosolic calcium levels in the presence of EGF, FIPI and Sig-1R agonists and antagonists as well as in PLD1 siRNA knockdown cells were determined by flow cytometry. Western blot analyses were performed to determine the basal expression levels and phosphorylation patterns of EGFR, HER2, AKT, MAPKp42/44, PLC-γ1 and Sig-1R. Results The EGF-induced migration of MDA-MB-468-NEO and MDA-MB-468-HER2 cells was significantly impaired by FIPI. Likewise, FIPI also significantly abolished EGF-induced calcium release in both cell lines. However, neither the expression levels nor the phosphorylation patterns of EGFR, HER2, AKT, MAPKp42/44 and PLC-γ1 were markedly changed by FIPI. Knockdown of PLD1 expression by siRNA also significantly impaired EGF-induced calcium release in both cell lines. Targeting Sig-1R, which interacts with IP3R, with the antagonist BD1047 also abrogated EGF-induced calcium release. However, EGF-induced calcium release was also impaired if cells were treated with the Sig-1R agonists PRE084 and PPBP maleate. Conclusion In summary, blocking PLD activity with the specific inhibitor FIPI or knocking down PDL1 expression by siRNA significantly impaired EGF-induced calcium release in MDA-MB-468-NEO and MDA-MB-468-HER2 cells, likely indicating a connection between PLD activity and PLC-γ1-mediated calcium signaling. However, how PLD activity interferes with the release of calcium from intracellular stores remains unclear.

Sign in / Sign up

Export Citation Format

Share Document