Multitargeted Nanoparticles Deliver Synergistic Drugs across the Blood–Brain Barrier to Brain Metastases of Triple Negative Breast Cancer Cells and Tumor‐Associated Macrophages

2019 ◽  
Vol 8 (18) ◽  
pp. 1900543 ◽  
Author(s):  
Tian Zhang ◽  
Hoyin Lip ◽  
Chunsheng He ◽  
Ping Cai ◽  
Zhigao Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Brain Metastases ◽  
Cancer Cells ◽  
Blood Brain Barrier ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Brain Barrier ◽  
Tumor Associated Macrophages ◽  
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 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

scholarly journals Disruption of the blood brain barrier by brain metastases of triple-negative and basal-type breast cancer but notHER2/neu-positive breast cancer

Cancer ◽  
2010 ◽  
Vol 116 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Kan Yonemori ◽  
Koji Tsuta ◽  
Makiko Ono ◽  
Chikako Shimizu ◽  
Akihiro Hirakawa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Brain Metastases ◽  
Blood Brain Barrier ◽  
Triple Negative ◽  
Brain Barrier ◽  
Blood Brain ◽  
Basal Type ◽  
Positive Breast Cancer

scholarly journals Sulforaphane Impacts Invasion Capacity and Proliferation of Triple Negative Breast Cancer Cells Grown in the Presence of Tumor-associated Macrophages (P05-003-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Katherine Jensen ◽  
Ed Slattery ◽  
Lauren Housley ◽  
Emilee Hansen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Vehicle Control ◽  
Tumor Associated Macrophages ◽  
Cell Counts ◽  
Proliferation And Invasion ◽  
Invasion Capacity

Abstract Objectives Triple negative breast cancer (TNBC) accounts for 12% to 24% of all breast cancer cases and is characterized by higher proliferation rates and an increased likelihood of tissue invasion. Tumor cells and cells in the tumor microenvironment (TME), specifically tumor associated macrophages (TAMs), interact through signaling (e.g., cytokines) to promote cancer progression by increasing proliferation and invasion capacity. Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables (i.e., broccoli) that has shown promising results in hindering TNBC progression. SFN reduced proliferation in breast cancer cells and altered cytokine signaling between breast cancer cells and cells in the TME (adipocytes). SFN also decreased invasion markers in TNBC cells grown in isolation. However, TAMs promote tumor cell aggression, and SFN's effect in multicellular environments is unclear. To determine SFN's potential in cancer treatment, it is critical to investigate SFN's effect on proliferation and invasion capacity of TNBC cells grown under TAMs influence, not just grown in isolation. The objective of this study was to determine if SFN can reduce proliferation and invasion capacity of TNBC cells grown in TAM secretions. Methods For cell proliferation, TNBC cells (MDA-MB-231) were exposed to TAM secretions using conditioned media and were then treated with SFN (10 μM) or DMSO vehicle control for 24 and 48 hours. Proliferation was measured using a MTT-based assay and cell counts. For invasion, TAMS and TNBC cells were co-cultured for 48 hours in transwell plates. Prior to co-culture period, cells were treated with SFN (15 μM) or vehicle control. Invasion capacity was measured through a transwell invasion assay with collagen representing the tumor basement membrane. ANOVA and t-tests were used to determine statistical differences with significance at P = 0.05. Results Preliminary analysis revealed significant reductions in proliferation for TAM exposed TNBC cells after 24 hours (P = 0. 0132) and 48 hours (P = 0. 0190) of SFN treatment. Conclusions SFN reduced proliferation and can potentially reduce invasion capacity of TNBC cells influenced by TAM secretions thus enhancing future utilization of SFN in TNBC treatment regimens. Funding Sources California State University, Chico.

scholarly journals Systemic HER3 ligand-mimicking bioparticles cross the blood–brain barrier reducing intracranial triple-negative breast cancer growth

2022 ◽  
Author(s):  
Felix Alonso-Valenteen ◽  
Sam Sances ◽  
HongQiang Wang ◽  
Simoun Mikhael ◽  
Jessica Sims ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Blood Brain Barrier ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Growth Factor Receptor ◽  
Metastatic Breast ◽  
Induced Pluripotent Stem Cell ◽  
Brain Barrier ◽  
Blood Brain ◽  
The Brain

Abstract Triple-negative breast cancer (TNBC) lacks selective biomarkers targeted by current clinical therapies and often metastasizes to the brain. Crossing the blood-brain barrier (BBB) and reaching intracranial tumors is a clinical challenge contributing to poor prognoses for patients. The human epidermal growth factor receptor HER3 has emerged as a biomarker of metastasis and may provide a means of therapeutically targeting TNBC. We have developed HER3-targeted biological particles (bioparticles) that exhibit systemic homing to resistant and metastatic breast tumors. Here we show that HER3 is expressed on the brain endothelium and can mediate the passage of bioparticles across the BBB and into intracranial TNBC. Our findings show that the extravasation of systemic bioparticles in mice and in human induced pluripotent stem cell-based BBB chips corresponds to HER3 levels. Furthermore, systemically delivered bioparticles carrying tumoricidal agents reduced the growth of intracranial TNBC in mice and exhibited improved therapeutic profile compared to current therapies.

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