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Nanoparticle Activation Methods in Cancer Treatment

White, Benjamin D, Duan, Chengchen, Townley, Helen E·2019·Biomolecules
DOI 10.3390/biom9050202PMC PMC6572460
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Abstract

In this review, we intend to highlight the progress which has been made in recent years around different types of smart activation nanosystems for cancer treatment. Conventional treatment methods, such as chemotherapy or radiotherapy, suffer from a lack of specific targeting and consequent off-target effects. This has led to the development of smart nanosystems which can effect specific regional and temporal activation. In this review, we will discuss the different methodologies which have been designed to permit activation at the tumour site. These can be divided into mechanisms which take advantage of the differences between healthy cells and cancer cells to trigger activation, and those which activate by a mechanism extrinsic to the cell or tumour environment.

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Figure 1 Graphic representation of the dissolution of dendrimer-cationized-albumin coated poly(lactic-co-glycolic-acid) (PLGA) nanoparticles. Doxorubicin (DOX) is released in the U-87 MG glioblastoma cells due to the pH of the acidic late endosomal compartment.
Figure 1 Graphic representation of the dissolution of dendrimer-cationized-albumin coated poly(lactic-co-glycolic-acid) (PLGA) nanoparticles. Doxorubicin (DOX) is released in the U-87 MG glioblastoma cells due to the pH of the acidic late endosomal compartment.CC BY · PubMed Central
Figure 2 Graphic representation of telomerase extending the 3’end aptamer which leads to the conformation change of the aptamer and release of the DOX inside tumour cells.
Figure 2 Graphic representation of telomerase extending the 3’end aptamer which leads to the conformation change of the aptamer and release of the DOX inside tumour cells.CC BY · PubMed Central
Figure 3 The singlet oxygen concentration was further enhanced by hCe6- hypoxia-activated prodrug (AQ4N)-liposome nanosystem irradiated by 660 nm laser and non-toxic AQ4N was transformed to toxic AQ4 by high concentration of singlet oxygen.
Figure 3 The singlet oxygen concentration was further enhanced by hCe6- hypoxia-activated prodrug (AQ4N)-liposome nanosystem irradiated by 660 nm laser and non-toxic AQ4N was transformed to toxic AQ4 by high concentration of singlet oxygen.CC BY · PubMed Central
Figure 4 Graphic representation of ultrasound stimulated piezoelectric stimulation of breast cancer cells. Upon ultrasound induced deformation, barium titanate nanoparticles create a potential difference that interferes with Ca2+ homeostasis and upregulates the Kir3.2 gene.
Figure 4 Graphic representation of ultrasound stimulated piezoelectric stimulation of breast cancer cells. Upon ultrasound induced deformation, barium titanate nanoparticles create a potential difference that interferes with Ca2+ homeostasis and upregulates the Kir3.2 gene.CC BY · PubMed Central
Figure 5 On-off tuneable release mechanism of chemotherapy molecules and gene therapy for DNA. The pores of the polymer reservoir are blocked by magnetic field susceptible ION nanoparticles.
Figure 5 On-off tuneable release mechanism of chemotherapy molecules and gene therapy for DNA. The pores of the polymer reservoir are blocked by magnetic field susceptible ION nanoparticles.CC BY · PubMed Central
Figure 6 Cell death mechanisms utilising different intensities of near infrared radiation (NIR) light for treating tumours at differing depths. At low penetration depths cell death is caused by reactive oxygen species (ROS) generated by Ce6 as photodynamic therapy (PDT). At high penetration depths and low light intensity cell death is caused by the release of docetaxel.
Figure 6 Cell death mechanisms utilising different intensities of near infrared radiation (NIR) light for treating tumours at differing depths. At low penetration depths cell death is caused by reactive oxygen species (ROS) generated by Ce6 as photodynamic therapy (PDT). At high penetration depths and low light intensity cell death is caused by the release of docetaxel.CC BY · PubMed Central

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Metadata

Authors
White, B. D., Duan, C., & Townley, H. E.
Venue
Biomolecules
Publisher
MDPI AG
Published
2019-05-24
Volume
9
Issue
5
Pages
202
ISSN
2218-273X
DOI
10.3390/biom9050202
PMC
PMC6572460
Cited by
32
References
0
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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CoChat. (2026). Citation check: Nanoparticle Activation Methods in Cancer Treatment. https://app.cochat.ai/papers/10.3390/biom9050202
The paper
White, B. D., Duan, C., & Townley, H. E. (2019). Nanoparticle Activation Methods in Cancer Treatment. Biomolecules. https://doi.org/10.3390/biom9050202