Cancer-Cell-Biomimetic Nanoparticles for Targeted Therapy of Homotypic Tumors

2016 ◽  
Vol 28 (43) ◽  
pp. 9581-9588 ◽  
Author(s):  
Huiping Sun ◽  
Jinghan Su ◽  
Qingshuo Meng ◽  
Qi Yin ◽  
Lingli Chen ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Cancer Cell ◽  
Biomimetic Nanoparticles

Cancer‐cell‐biomimetic Nanoparticles for Targeted Therapy of Multiple Myeloma Based on Bone Marrow Homing

2021 ◽  
pp. 2107883
Author(s):  
Ying Qu ◽  
Bingyang Chu ◽  
Xue Wei ◽  
Yingying Chen ◽  
Yun Yang ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Targeted Therapy ◽  
Cancer Cell ◽  
Biomimetic Nanoparticles

Cell membrane based biomimetic nanocomposites for targeted therapy of drug resistant EGFR-mutated lung cancer

Nanoscale ◽  
2019 ◽  
Vol 11 (41) ◽  
pp. 19520-19528 ◽  
Author(s):  
Pengying Wu ◽  
Dongtao Yin ◽  
Jiaming Liu ◽  
Huige Zhou ◽  
Mengyu Guo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Targeted Therapy ◽  
Cell Membrane ◽  
Cancer Cell ◽  
Egfr Mutation ◽  
Drug Resistant ◽  
Egfr Mutated

A cancer cell membrane-based biomimetic strategy was developed by loading doxorubicin and icotinib to overcome drug-resistance of EGFR-mutation lung cancer.

scholarly journals Human Cancer Cell Membrane-Coated Biomimetic Nanoparticles Reduce Fibroblast-Mediated Invasion and Metastasis and Induce T-Cells

2019 ◽  
Vol 11 (8) ◽  
pp. 7850-7861 ◽  
Author(s):  
Jiefu Jin ◽  
Balaji Krishnamachary ◽  
James D. Barnett ◽  
Samit Chatterjee ◽  
Di Chang ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Membrane ◽  
Cancer Cell ◽  
Human Cancer ◽  
Human Cancer Cell ◽  
Invasion And Metastasis ◽  
Biomimetic Nanoparticles

Genomic-directed targeted therapy increases endometrial cancer cell sensitivity to doxorubicin

2010 ◽  
Vol 203 (2) ◽  
pp. 158.e1-158.e40 ◽  
Author(s):  
Megan D. Indermaur ◽  
Yin Xiong ◽  
Siddharth G. Kamath ◽  
Todd Boren ◽  
Ardeshir Hakam ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Targeted Therapy ◽  
Cancer Cell ◽  
Cell Sensitivity ◽  
Endometrial Cancer Cell

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...

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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