scholarly journals Lipid-Based Nanovectors for Targeting of CD44-Overexpressing Tumor Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Silvia Arpicco ◽  
Giuseppe De Rosa ◽  
Elias Fattal

Hyaluronic acid (HA) is a naturally occurring glycosaminoglycan that exists in living systems, and it is a major component of the extracellular matrix. The hyaluronic acid receptor CD44 is found at low levels on the surface of epithelial, haematopoietic, and neuronal cells and is overexpressed in many cancer cells particularly in tumour initiating cells. HA has been therefore used as ligand attached to HA-lipid-based nanovectors for the active targeting of small or large active molecules for the treatment of cancer. This paper describes the different approaches employed for the preparation, characterization, and evaluation of these potent delivery systems.

ACS Omega ◽  
2021 ◽  
Author(s):  
Yu-Yu Aung ◽  
Aswandi Wibrianto ◽  
Jefry S. Sianturi ◽  
Desita K. Ulfa ◽  
Satya. C. W. Sakti ◽  
...  

RSC Advances ◽  
2015 ◽  
Vol 5 (58) ◽  
pp. 46464-46479 ◽  
Author(s):  
Yan Shen ◽  
Jue Wang ◽  
Yanan Li ◽  
Yu Tian ◽  
Huimin Sun ◽  
...  

Schematic diagram showing the structure of the co-delivery nano-complex and the process of entering tumor cells.


2009 ◽  
Vol 6 (4) ◽  
pp. 1062-1073 ◽  
Author(s):  
Claudio Surace ◽  
Silvia Arpicco ◽  
Amélie Dufaÿ-Wojcicki ◽  
Véronique Marsaud ◽  
Céline Bouclier ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mohammad Imran Khan ◽  
Mazin A. Zamzami ◽  
Aftab Ahmad ◽  
Hani Choudhry

AbstractDuring cancer, a major challenge faced by oncologists is the treatment of metastasis; a leading cause of cancer-related deaths around the world. Metastasis involves a highly ordered sequence of events starting with the detachment of tumor cells from the extracellular matrix (E.C.M.). In normal cells, detachment from E.C.M. triggers programmed cell death, termed anoikis. However, tumor cells dodge their way to anoikis and spread to distant sites for initiating the metastatic program. In this work, we explored the impact of E.C.M. detachment on the expression of some major oncogenic histone methyltransferases. Results showed both EZH2 expression and its enzymatic activity were significantly increased in E.C.M. detached cancer cells when compared to the attached cells. Inhibition of EZH2 results in a significant reduction in cell proliferation, spheroids size, and induction in apoptosis in E.C.M. detached cells. Furthermore, we observed a reduction in EZH2 expression levels in single cells when compared to clusters of E.C.M. detached cells. Finally, we combined the EZH2 inhibition with AMPK, known to be highly expressed in E.C.M. detached cancer cells and observed antagonistic effects between the two pathways. The observed results clearly showed that E.C.M. detached cancer cells require oncogenic EZH2 and can be targeted by EZH2 inhibitors.


Micromachines ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1018
Author(s):  
Chang Ryong Lee ◽  
Gun Gyun Kim ◽  
Sung Bum Park ◽  
Sang Wook Kim

This study is based on the principle that superparamagnetic iron oxide nanoparticles (Fe3O4) can be used to target a specific area given that their magnetic properties emerge when an external magnetic field is applied. Cerium oxide (CeO2), which causes oxidative stress by generating reactive oxygen species (ROS) in the environment of tumor cells, was synthesized on the surface of superparamagnetic iron oxide nanoparticles to produce nanoparticles that selectively kill cancer cells. In addition, hyaluronic acid (HA) was coated on the cerium’s surface to target CD44-overexpressing tumor cells, and natZr was chelated on the Fe3O4@CeO2 surface to show the usefulness of labeling the radioisotope 89Zr (T1/2 = 3.3 d). The synthesis of Fe3O4@CeO2 was confirmed by Fourier Transform-Infrared Spectroscopy (FT-IR), X-ray Diffraction (XRD) and Field Emission-Transmission Electron Microscope (FE-TEM). The coating of HA was confirmed by FT-IR, X-ray Photoelectron. Spectroscopy (XPS), FE-TEM, Energy-Dispersive X-ray Spectroscopy (EDS) and Thermogravimetric Analysis (TGA)/Differential Scanning Calorimetry (DSC). The sizes of the prepared nanoparticles were confirmed through FE-TEM and Field Emission-Scanning Electron (FE-SEM) (sizes of 15 to 30 nm), and it was confirmed that natZr was introduced onto the surface of the nanoparticles using EDS. The particle size of the dispersed material was limited through Dynamic Light Scattering (DLS) to about 148 nm in aqueous solution, which was suitable for the (enhanced permeation and retention) EPR effect. It was confirmed that the HA-coated nanoparticles have good dispersibility. Finally, a cytotoxicity evaluation confirmed the ability of CeO2 to generate ROS and target the delivery of HA. In conclusion, Fe3O4@CeO2 can effectively inhibit cancer cells through the activity of cerium oxide in the body when synthesized in nano-sized superparamagnetic coral iron that has magnetic properties. Subsequently, by labeling the radioactive isotope 89Zr, it is possible to create a theranostic drug delivery system that can be used for cancer diagnosis.


Author(s):  
Jin G. Jung ◽  
Anne Le

AbstractThe tumor microenvironment (TME) is a complex biological structure surrounding tumor cells and includes blood vessels, immune cells, fibroblasts, adipocytes, and extracellular matrix (ECM) [1, 2]. These heterogeneous surrounding structures provide nutrients, metabolites, and signaling molecules to provide a cancer-friendly environment. The metabolic interplay between immune cells and cancer cells in the TME is a key feature not only for understanding tumor biology but also for discovering cancer cells’ vulnerability. As cancer immunotherapy to treat cancer patients and the use of metabolomics technologies become more and more common [3], the importance of the interplay between cancer cells and immune cells in the TME is emerging with respect to not only cell-to-cell interactions but also metabolic pathways. This interaction between immune cells and cancer cells is a complex and dynamic process in which immune cells act as a determinant factor of cancer cells’ fate and vice versa. In this chapter, we provide an overview of the metabolic interplay between immune cells and cancer cells and discuss the therapeutic opportunities as a result of this interplay in order to define targets for cancer treatment. It is important to understand and identify therapeutic targets that interrupt this cancerpromoting relationship between cancer cells and the surrounding immune cells, allowing for maximum efficacy of immune checkpoint inhibitors as well as other genetic and cellular therapies.


Nanoscale ◽  
2017 ◽  
Vol 9 (33) ◽  
pp. 12150-12162 ◽  
Author(s):  
Talitha F. Stefanello ◽  
Benoit Couturaud ◽  
Anna Szarpak-Jankowska ◽  
David Fournier ◽  
Benoit Louage ◽  
...  

Light- and thermoresponsive hyaluronic acid-based nanogels carry hydrophobic molecules to cancer cells.


Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6548
Author(s):  
Wen-Jui Lee ◽  
Shih-Hsin Tu ◽  
Tzu-Chun Cheng ◽  
Juo-Han Lin ◽  
Ming-Thau Sheu ◽  
...  

The microenvironment for tumor growth and developing metastasis should be essential. This study demonstrated that the hyaluronic acid synthase 3 (HAS3) protein and its enzymatic product hyaluronic acid (HA) encompassed in the subcutaneous extracellular matrix can attenuate the invasion of human breast tumor cells. Decreased HA levels in subcutaneous Has3-KO mouse tissues promoted orthotopic breast cancer (E0771) cell-derived allograft tumor growth. MDA-MB-231 cells premixed with higher concentration HA attenuate tumor growth in xenografted nude mice. Human patient-derived xenotransplantation (PDX) experiments found that HA selected the highly migratory breast cancer cells with CD44 expression accumulated in the tumor/stroma junction. In conclusion, HAS3 and HA were detected in the stroma breast tissues at a high level attenuates effects for induced breast cancer cell death, and inhibit the cancer cells invasion at the initial stage. However, the highly migratory cancer cells were resistant to the HA-mediated effects with unknown mechanisms.


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