Targeted imaging and targeted therapy of breast cancer cells via fluorescent double template-imprinted polymer coated silicon nanoparticles by an epitope approach

Nanoscale ◽  
2019 ◽  
Vol 11 (36) ◽  
pp. 17018-17030 ◽  
Author(s):  
Hai-Yan Wang ◽  
Pei-Pei Cao ◽  
Zheng-Ying He ◽  
Xi-Wen He ◽  
Wen-You Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Silicon Nanoparticles ◽  
Targeted Imaging ◽  
Imprinted Polymer ◽  
Fluorescence Diagnosis ◽  
Specific Fluorescence ◽  
Epitope Approach

Dual-template imprinted polymer coated silicon nanoparticles with epitope imprinting achieved specific fluorescence diagnosis and targeted therapy of breast cancer cells.

scholarly journals Aptamer-protamine-siRNA nanoparticles in targeted therapy of ErbB3 positive breast cancer cells

2020 ◽  
Vol 590 ◽  
pp. 119963
Author(s):  
Xiangshang Xu ◽  
Li Li ◽  
Xiaolan Li ◽  
Deding Tao ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Positive Breast Cancer

Selective chemotherapy and imaging of colorectal and breast cancer cells by a modified MUC-1 aptamer conjugated to a poly(ethylene glycol)-dimethacrylate coated Fe3O4–AuNCs nanocomposite

2019 ◽  
Vol 43 (1) ◽  
pp. 238-248 ◽  
Author(s):  
Roya Binaymotlagh ◽  
Farid Hajareh Haghighi ◽  
Fatemeh Aboutalebi ◽  
Seyede Zohreh Mirahmadi-Zare ◽  
Hassan Hadadzadeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Ethylene Glycol ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Molecular Medicine ◽  
Glycol Dimethacrylate ◽  
Poly Ethylene Glycol ◽  
Poly Ethylene ◽  
Selective Chemotherapy

The combination of diagnosis and targeted therapy within a single nanoplatform is one of the remarkable advances in molecular medicine.

Supramolecular assembly of fluorogenic glyco-dots from perylenediimide-based glycoclusters for targeted imaging of cancer cells

2017 ◽  
Vol 53 (87) ◽  
pp. 11937-11940 ◽  
Author(s):  
Ying Liu ◽  
Ding-Kun Ji ◽  
Lei Dong ◽  
Nicolas Galanos ◽  
Yi Zang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Self Assembly ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Supramolecular Assembly ◽  
Targeted Imaging

Supramolecular self-assembly between perylenediimide-based glycoclusters and a red-emitting fluorophore produces structurally uniform and stable glyco-dots amenable to targeted fluorogenic imaging of liver and triple-negative breast cancer cells.

scholarly journals Photostable and Biocompatible Fluorescent Silicon Nanoparticles for Imaging-Guided Co-Delivery of siRNA and Doxorubicin to Drug-Resistant Cancer Cells

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Daoxia Guo ◽  
Xiaoyuan Ji ◽  
Fei Peng ◽  
Yiling Zhong ◽  
Binbin Chu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Rna Interference ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Silicon Nanoparticles ◽  
Multidrug Resistant ◽  
Rnase A ◽  
Drug Resistant ◽  
Fluorescent Silicon Nanoparticles ◽  
P Glycoprotein

Abstract The development of effective and safe vehicles to deliver small interfering RNA (siRNA) and chemotherapeutics remains a major challenge in RNA interference-based combination therapy with chemotherapeutics, which has emerged as a powerful platform to treat drug-resistant cancer cells. Herein, we describe the development of novel all-in-one fluorescent silicon nanoparticles (SiNPs)-based nanomedicine platform for imaging-guided co-delivery of siRNA and doxorubicin (DOX). This approach enhanced therapeutic efficacy in multidrug-resistant breast cancer cells (i.e., MCF-7/ADR cells). Typically, the SiNP-based nanocarriers enhanced the stability of siRNA in a biological environment (i.e., medium or RNase A) and imparted the responsive release behavior of siRNA, resulting in approximately 80% down-regulation of P-glycoprotein expression. Co-delivery of P-glycoprotein siRNA and DOX led to > 35-fold decrease in the half maximal inhibitory concentration of DOX in comparison with free DOX, indicating the pronounced therapeutic efficiency of the resultant nanocomposites for drug-resistant breast cancer cells. The intracellular time-dependent release behaviors of siRNA and DOX were revealed through tracking the strong and stable fluorescence of SiNPs. These data provide valuable information for designing effective RNA interference-based co-delivery carriers.

Susceptibility of HER2+ breast cancer cells to poly (ADP-ribose) polymerase (PARP) inhibition independent of an inherent DNA repair defect.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 621-621 ◽  
Author(s):  
Eddy Shih-Hsin Yang ◽  
Somaira Nowsheen ◽  
Tiffiny Cooper ◽  
Albert F. LoBuglio ◽  
James A. Bonner
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Parp Inhibition ◽  
Growth Delay ◽  
Her2 Overexpression ◽  
Tumor Growth Delay ◽  
Her2 Breast Cancer

621 Background: HER2 overexpression in breast cancer confers increased tumor aggressiveness. Targeted therapy against HER2 has improved outcomes, but resistance and disease progression ultimately occurs, thus necessitating novel therapeutic strategies. PARP inhibitors target homologous recombination (HR) deficient tumors, such as the BRCA-associated breast and ovarian cancers. In this study, we report unexpected susceptibility of HER2+ breast cancer cells to PARP inhibition alone independent of an inherent HR deficiency. Methods: Cell viability was measured using colony formation and ATPLite assays. Tumor growth delay was assessed in vivo in mice bearing breast cancer xenografts. Proteins were detected by immunoblotting. HR was assayed using radiation (IR)-induced Rad51 foci or a GFP-based HR assay. NFκB activity was measured using a NFκB-driven luciferase assay. Results: Surprisingly, PARP inhibition with ABT-888 alone reduced the colony forming ability and cell viability of the HER2+ breast cancer cell lines BT474, SKBR3, MDA-MB361, and HCC1954 (~70 – 99% reduction at 10μM). This susceptibility did not correlate with an inherent HR deficit. Interestingly, HER2 overexpression itself may be one mechanism of susceptibility to ABT-888 as evidenced by increased cellular cytotoxicity and in vivo tumor growth delay of MCF7 cells stably expressing HER2. Further dissection of the mechanism revealed that NFκB transcriptional activity was significantly inhibited by ABT-888 (>95%) which corresponded with reduced levels of phosphorylated p65 and total IKKα, and a concomitant increase in IkBα. Furthermore, overexpression of p65 abrogated cellular sensitivity to ABT-888. Conclusions: HER2+ breast cancer cells are highly susceptible to PARP inhibition despite being HR proficient. This may be, in part, due to inhibition of NFκB. Further investigation of whether the addition of PARP inhibition to HER2 targeted therapy will delay the onset of resistance to therapy is warranted to potentially improve outcomes in HER2+ breast cancer patients.

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