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Review
. 2020 Mar 11;10(3):504.
doi: 10.3390/nano10030504.

The Rational Design and Biological Mechanisms of Nanoradiosensitizers

Hainan Sun  1   2 , Xiaoling Wang  1 , Shumei Zhai  1
Affiliations
Review

The Rational Design and Biological Mechanisms of Nanoradiosensitizers

Hainan Sun et al. Nanomaterials (Basel). .

Abstract

Radiotherapy (RT) has been widely used for cancer treatment. However, the intrinsic drawbacks of RT, such as radiotoxicity in normal tissues and tumor radioresistance, promoted the development of radiosensitizers. To date, various kinds of nanoparticles have been found to act as radiosensitizers in cancer radiotherapy. This review focuses on the current state of nanoradiosensitizers, especially the related biological mechanisms, and the key design strategies for generating nanoradiosensitizers. The regulation of oxidative stress, DNA damage, the cell cycle, autophagy and apoptosis by nanoradiosensitizers in vitro and in vivo is highlighted, which may guide the rational design of therapeutics for tumor radiosensitization.

Keywords: biological mechanisms; nanoradiosensitizers; physicochemical properties; radiosensitization; radiotherapy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Enhanced radiosensitivity of cancer cells by gold nanoclusters (AuNCs) with mitochondria targeting. Peptide-templated AuNCs were synthesized through a green synthetic route, featured with highly efficient co-localization onto mitochondria after endocytosis. Under 4 Gy X-ray irradiation, peptide (CCYKFR)–AuNCs can introduce the burst of mitoROS and cell death. Reproduced with permission [30]. Copyright The Royal Society of Chemistry, 2017.
Figure 2
Figure 2
Multifunctional nanosphere for combined chemo-radiotherapy. Principle of nanosphere action based on gold and platinum mediated radiosensitization and cisplatin induced genotoxic damage. Reproduced with permission [85]. Copyright The Royal Society of Chemistry, 2014.
Figure 3
Figure 3
Preparation of MTiO2(SN-38)- transactivator of transcription (TAT)-Arg-Gly-Asp (RGD) nanoparticles (NPs) and its application for enhanced radiotherapy. Reproduced with permission [127]. Copyright The Royal Society of Chemistry, 2019.
Figure 4
Figure 4
Mitochondria-targeted radiotherapy (RT)-radiodynamic therapy (RDT) mediated by Hf-DBB-Ru. Hf-DBB-Ru was internalized by tumor cells efficiently and enriched in mitochondria due to dispersed cationic charges in the nMOF framework. Hf6 SBUs preferentially absorb X-rays over tissues to enhance RT by sensitizing hydroxyl radical generation and enable RDT by transferring energy to Ru(bpy)32+-based bridging ligands to generate singlet oxygen. The RT-RDT process trigger mitochondrial membrane potential depolarization, membrane integrity loss, respiratory chain inactivation, and cytochrome c release to initiate apoptosis of cancer cells. Reproduced with permission. Copyright Springer Nature, 2018.
Figure 5
Figure 5
The mechanism and signaling pathways in autophagy induced by cetyl trimethyl ammonium bromide gold nanorods (CTAB-GNRs) and polystyrene sulfonate gold nanorods ( PSS-GNRs). Reproduced with permission [185]. Copyright The Royal Society of Chemistry, 2015.
Figure 6
Figure 6
Biological mechanisms involved in NPs’ radiosensitization.
See this image and copyright information in PMC

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