scholarly journals The proinflammatory peptide substance P promotes blood–brain barrier breaching by breast cancer cells through changes in microvascular endothelial cell tight junctions

2013 ◽  
Vol 134 (5) ◽  
pp. 1034-1044 ◽  
Author(s):  
Pedro L. Rodriguez ◽  
Shuxian Jiang ◽  
Yigong Fu ◽  
Shalom Avraham ◽  
Hava Karsenty Avraham
Keyword(s):  
Breast Cancer ◽  
Endothelial Cell ◽  
Substance P ◽  
Cancer Cells ◽  
Tight Junctions ◽  
Blood Brain Barrier ◽  
Breast Cancer Cells ◽  
Brain Barrier ◽  
Microvascular Endothelial Cell ◽  
Blood Brain

Angiopoietin-2 mediates blood-brain barrier impairment and colonization of triple-negative breast cancer cells in brain

2014 ◽  
Vol 232 (3) ◽  
pp. 369-381 ◽  
Author(s):  
Hava Karsenty Avraham ◽  
Shuxian Jiang ◽  
Yigong Fu ◽  
Harikrishna Nakshatri ◽  
Haim Ovadia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Blood Brain Barrier ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Brain Barrier ◽  
Blood Brain ◽  
Angiopoietin 2

scholarly journals ST6GALNAC5 Expression Decreases the Interactions between Breast Cancer Cells and the Human Blood-Brain Barrier

2016 ◽  
Vol 17 (8) ◽  
pp. 1309 ◽  
Author(s):  
Aurore Drolez ◽  
Elodie Vandenhaute ◽  
Clément Delannoy ◽  
Justine Dewald ◽  
Fabien Gosselet ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Blood Brain Barrier ◽  
Human Blood ◽  
Breast Cancer Cells ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Effect of heat stress on blood-brain barrier integrity in iPS cell-derived microvascular endothelial cell models

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222113 ◽  
Author(s):  
Tomoko Yamaguchi ◽  
Kentaro Shimizu ◽  
Yasuhiro Kokubu ◽  
Misae Nishijima ◽  
Shuko Takeda ◽  
...  
Keyword(s):  
Heat Stress ◽  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Microvascular Endothelial Cell ◽  
Cell Models ◽  
Ips Cell ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Blood Brain Barrier Integrity

scholarly journals Functional inhibition of F11 receptor (F11R/junctional adhesion molecule-A/JAM-A) activity by a F11R-derived peptide in breast cancer and its microenvironment

2019 ◽  
Vol 179 (2) ◽  
pp. 325-335 ◽  
Author(s):  
Radoslaw Bednarek ◽  
Anna Selmi ◽  
Dagmara Wojkowska ◽  
Kamil Karolczak ◽  
Marcin Popielarski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endothelial Cell ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Cell Surface Expression ◽  
Microvascular Endothelial Cell

Abstract Purpose To examine the involvement of the F11R/JAM-A protein in breast cancer metastasis, we utilized the F11R/JAM-A antagonistic peptide 4D (P4D) in experiments of transendothelial migration (TEM) of breast cancer cells. Methods Experiments were conducted in the mouse 4T1 breast cancer model utilizing the human mammary epithelial cell and endothelial cell lines. The levels of soluble F11R/JAM-A (sJAM-A) in the murine plasmas were measured by ELISA. Levels of F11R/JAM-A mRNA and protein in cell lines were assessed by qRT-PCR and Western blot, respectively. Cell surface expression of F11R/JAM-A was demonstrated by flow cytometry. Functional tests included the TEM of breast cancer cells and adhesion of breast cancer cells to the endothelium. The endothelial permeability was studied by fluorescent tracer assay and by the Real-Time Cell Analysis (RTCA). Results The tumor inducers Tβ4 and TGF-β1 reduced the levels of sJAM-A in murine plasma, and reduced the F11R/JAM-A protein levels in the human microvascular endothelial cell line HMEC-1. The adhesion and TEM measured between breast cancer cells and inflamed or Tβ4-treated endothelium were inhibited by P4D. The presence of P4D did not destabilize the pre-existing tight junctions in the endothelial monolayer. The barrier-protecting effect of P4D was stronger than that of forskolin, when a booster dose of P4D was applied to the inflamed endothelium. Conclusions F11R/JAM-A protein can be considered as a novel target in the treatment of breast cancer metastasis. In vivo and clinical studies are needed to further investigate the effectiveness of F11R/JAM-A-derived peptide as a possible anti-metastatic drug.

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