Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells

10.3791/62249 ◽  
2021 ◽  
Author(s):  
Xiaoding Hu ◽  
Emilly S. Villodre ◽  
Wendy A. Woodward ◽  
Bisrat G. Debeb
Keyword(s):  
Breast Cancer ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Inflammatory Breast Cancer ◽  
Breast Cancer Cells ◽  
Tail Vein ◽  
Tail Vein Injection

scholarly journals Proteotranscriptomic Profiling of 231-BR Breast Cancer Cells: Identification of Potential Biomarkers and Therapeutic Targets for Brain Metastasis

2015 ◽  
Vol 14 (9) ◽  
pp. 2316-2330 ◽  
Author(s):  
Matthew D. Dun ◽  
Robert J. Chalkley ◽  
Sam Faulkner ◽  
Sheridan Keene ◽  
Kelly A. Avery-Kiejda ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Targets ◽  
Potential Biomarkers

scholarly journals miR-509 suppresses brain metastasis of breast cancer cells by modulating RhoC and TNF-α

Oncogene ◽  
2015 ◽  
Vol 34 (37) ◽  
pp. 4890-4900 ◽  
Author(s):  
F Xing ◽  
S Sharma ◽  
Y Liu ◽  
Y-Y Mo ◽  
K Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tnf Α

Dominant-negative E-cadherin inhibits the invasiveness of inflammatory breast cancer cells in vitro

2006 ◽  
Vol 133 (2) ◽  
pp. 83-92 ◽  
Author(s):  
Hui-Ming Dong ◽  
Gang Liu ◽  
Yi-Feng Hou ◽  
Jiong Wu ◽  
Jin-Song Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Inflammatory Breast Cancer ◽  
Breast Cancer Cells ◽  
Dominant Negative ◽  
E Cadherin

scholarly journals BSCI-25. THE ROLE OF THE IFNγ PATHWAY IN BREAST CANCER BRAIN METASTASIS FORMATION

2019 ◽  
Vol 1 (Supplement_1) ◽  
pp. i5-i5
Author(s):  
Route Pedrosa ◽  
Benjamin Schrijver ◽  
Rute B Marques ◽  
Pieter J M Leenen ◽  
Wim A Dik ◽  
...  
Keyword(s):  
Breast Cancer ◽  
T Lymphocytes ◽  
Brain Metastasis ◽  
Brain Metastases ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
T Cell Response ◽  
Activated T Cells ◽  
Breast Cancer Brain Metastasis

Abstract In previous work, we showed the prominence of the T cell response in the formation of brain metastases of primary ER-negative breast cancers. We also showed that prior co-cultured breast cancer cells with stimulated T lymphocytes bear an overexpression of Guanylate-binding protein 1 (GBP1) and possess an increased trespassing ability through an in vitro blood-brain barrier (BBB) model. In addition, we demonstrated a predilection for metastasizing to the brain of breast cancer cells that were co-cultured with activated T cells in a mouse model. In the present work, we show that activated CD8+ cytotoxic T lymphocytes, rather than CD4+ lymphocytes, are the main cause of increasing the ability of breast cancer cells to cross the BBB. While synthetic IFNγ does not change the ability of breast cancer cells to cross the BBB, this study shows that the T lymphocyte-secreted IFNγ activates the STAT1-dependent IFNγ pathway in breast cancer cells, enabling them to cross the in vitro BBB. Direct inhibition of soluble IFNγ or blocking of the IFNγ-specific receptor in breast cancer cells significantly decreases their ability to cross the BBB. The results illustrate that IFNγ signaling pathway is one of the crucial pathways in the formation of brain metastasis of ER- breast cancer. The interference with the IFNγ pathway will develop preventive strategies against the formation of brain metastases of breast cancer.

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