Multi-functional DNA-conjugated nanohydrogels for aptamer-directed breast cancer cell targeting

2021 ◽  
Author(s):  
Gangfeng Jiang ◽  
Nannan Wang ◽  
Lina Jia ◽  
Hongli Che ◽  
Lihui Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Targeting ◽  
Conjugation Chemistry ◽  
Cancer Cell Targeting ◽  
Functional Dna

The development of new conjugation chemistry involving DNA and nanoparticles as well as nanoparticle-based platforms for aptamer-directed cancer-cell targeting is important for improved targeted therapy and imaging. Herein, a dual...

⿿Blind⿿ targeting in action: From phage display to breast cancer cell targeting with peptide-gold nanoconjugates

2016 ◽  
Vol 111 ◽  
pp. 155-162 ◽  
Author(s):  
Elisabetta Galbiati ◽  
Luca Gambini ◽  
Viola Civitarese ◽  
Michela Bellini ◽  
Dario Ambrosini ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Phage Display ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Targeting ◽  
Cancer Cell Targeting

Proteolytically Stable Cyclic Decapeptide for Breast Cancer Cell Targeting

2017 ◽  
Vol 60 (12) ◽  
pp. 4893-4903 ◽  
Author(s):  
Yogita Raghuwanshi ◽  
Hashem Etayash ◽  
Rania Soudy ◽  
Igor Paiva ◽  
Afsaneh Lavasanifar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Targeting ◽  
Cancer Cell Targeting

mAb-Labeled Liposomes in Breast Cancer Cell Targeting.

1993 ◽  
Vol 698 (1 Breast Cancer) ◽  
pp. 429-435 ◽  
Author(s):  
G. ROMBI ◽  
F. COSSU ◽  
G. MELIS
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Targeting ◽  
Cancer Cell Targeting

d -Fructose-Decorated Poly(ethylene imine) for Human Breast Cancer Cell Targeting

2017 ◽  
Vol 17 (8) ◽  
pp. 1600502 ◽  
Author(s):  
Christoph Englert ◽  
Michael Pröhl ◽  
Justyna A. Czaplewska ◽  
Carolin Fritzsche ◽  
Elisabeth Preußger ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Cell Targeting ◽  
Human Breast ◽  
Ethylene Imine ◽  
Cancer Cell Targeting ◽  
Poly Ethylene

scholarly journals Breast Cancer Cell Targeting by Prenylation Inhibitors Elucidated in Living Animals with a Bioluminescence Reporter

2012 ◽  
Vol 18 (15) ◽  
pp. 4136-4144 ◽  
Author(s):  
Sharon L. Chinault ◽  
Julie L. Prior ◽  
Kevin M. Kaltenbronn ◽  
Anya Penly ◽  
Katherine N. Weilbaecher ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Targeting ◽  
Cancer Cell Targeting

scholarly journals A SNAI2-PEAK1-INHBA stromal axis drives progression and lapatinib resistance in HER2-positive breast cancer by supporting subpopulations of tumor cells positive for antiapoptotic and stress signaling markers

Oncogene ◽  
2021 ◽  
Author(s):  
Sarkis Hamalian ◽  
Robert Güth ◽  
Farhana Runa ◽  
Francesca Sanchez ◽  
Eric Vickers ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Metastasis ◽  
Dependent Manner ◽  
Her2 Positive ◽  
Cell Axis ◽  
Her2 Positive Breast Cancer ◽  
Positive Breast Cancer

AbstractIntercellular mechanisms by which the stromal microenvironment contributes to solid tumor progression and targeted therapy resistance remain poorly understood, presenting significant clinical hurdles. PEAK1 (Pseudopodium-Enriched Atypical Kinase One) is an actin cytoskeleton- and focal adhesion-associated pseudokinase that promotes cell state plasticity and cancer metastasis by mediating growth factor-integrin signaling crosstalk. Here, we determined that stromal PEAK1 expression predicts poor outcomes in HER2-positive breast cancers high in SNAI2 expression and enriched for MSC content. Specifically, we identified that the fibroblastic stroma in HER2-positive breast cancer patient tissue stains positive for both nuclear SNAI2 and cytoplasmic PEAK1. Furthermore, mesenchymal stem cells (MSCs) and cancer-associated fibroblasts (CAFs) express high PEAK1 protein levels and potentiate tumorigenesis, lapatinib resistance and metastasis of HER2-positive breast cancer cells in a PEAK1-dependent manner. Analysis of PEAK1-dependent secreted factors from MSCs revealed INHBA/activin-A as a necessary factor in the conditioned media of PEAK1-expressing MSCs that promotes lapatinib resistance. Single-cell CycIF analysis of MSC-breast cancer cell co-cultures identified enrichment of p-Akthigh/p-gH2AXlow, MCL1high/p-gH2AXlow and GRP78high/VIMhigh breast cancer cell subpopulations by the presence of PEAK1-expressing MSCs and lapatinib treatment. Bioinformatic analyses on a PEAK1-centric stroma-tumor cell gene set and follow-up immunostaining of co-cultures predict targeting antiapoptotic and stress pathways as a means to improve targeted therapy responses and patient outcomes in HER2-positive breast cancer and other stroma-rich malignancies. These data provide the first evidence that PEAK1 promotes tumorigenic phenotypes through a previously unrecognized SNAI2-PEAK1-INHBA stromal cell axis.

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