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

scholarly journals Systemic Sclerosis-Endothelial Cell Antiangiogenic Pentraxin 3 and Matrix Metalloprotease 12 Control Human Breast Cancer Tumor Vascularization and Development in Mice

Neoplasia ◽  
2009 ◽  
Vol 11 (10) ◽  
pp. 1106-1115 ◽  
Author(s):  
Francesca Margheri ◽  
Simona Serratì ◽  
Andrea Lapucci ◽  
Chillà Anastasia ◽  
Betti Giusti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Systemic Sclerosis ◽  
Endothelial Cell ◽  
Human Breast Cancer ◽  
Pentraxin 3 ◽  
Matrix Metalloprotease ◽  
Human Breast ◽  
Tumor Vascularization ◽  
Cancer Tumor

High expression of TIMP-1 in human breast cancer tissues is a predictive of resistance to paclitaxel-based chemotherapy

2012 ◽  
Vol 29 (5) ◽  
pp. 3207-3215 ◽  
Author(s):  
Dongliang Zhu ◽  
Xiaoming Zha ◽  
Meiling Hu ◽  
Aidi Tao ◽  
Hangbo Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
High Expression ◽  
Human Breast ◽  
Cancer Tissues

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.

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