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Effects of Ionizing Radiation in Cancer Radiotherapy: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (25 April 2025) | Viewed by 1155

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UMR6252 CIMAP, CEA-CNRS-ENSICAEN, Normandie Université, Team Applications in Radiobiology with Accelerated Ions, 14000 Caen, France
Interests: cancer cell biology; radiotherapy; particle therapy; DNA damage response; signaling transduction; radiation-induced bystander effects; tumor cell radio-sensitization; integrated omics; proteomics; radiation response biomarkers; radioresistance; combined treatments; tumor microenvironment; inflammatory
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Dear Colleagues,

For a long time, it has been widely accepted that biological effects of ionizing radiation, such as cell death, DNA damage, and mutagenesis, result from direct ionization of cell structures, particularly DNA, or from indirect damage through reactive oxygen species produced by radiolysis of water. This “targeted effect” (TE) model has been questioned by numerous observations in which cells that were not directly irradiated exhibited responses similar to those of the directly irradiated cells. Therefore, it is currently accepted that ionizing radiation's detrimental effects are restricted to the irradiated cells and non-irradiated adjacent or distant cells.

Non-targeted effects (NTEs) of ionizing radiation, which include genomic instability, radiation-induced bystander effects, and abscopal effects, are defined as the occurrence of biological effects in non-irradiated cells because of irradiation of other cells in the population. In opposition to TEs, which display a linear dose–response, NTEs exhibit a non-linear dose–response with a marked effect at low doses of radiation. NTE-related cellular and molecular mechanisms are still not completely understood, as they mainly depend on the cell type and the radiation quality. It is now widely admitted that irradiated cells produce stress factors in specific conditions, which affect non-irradiated cells in the close environment (Bystander effect) or at a distance (Abscopal effect). The cellular response observed in non-irradiated cells can be very similar to the response of irradiated cells, with a modulated intensity. NTEs involve the secretion or the release by irradiated cells of a broad range of stress factors, from cytokines and specifically secreted molecules to reactive oxygen species or oxidized cellular wastes. In the case of communication between neighborhood cells, the stress factors can disseminate through gap junctions or, in the case of distance communication, through small vesicles containing various embedded molecules. NTEs are commonly studied as low-dose radiation effects in radioprotection, in association with genomic instability, mutation induction, and secondary cancer risk.

In a radiotherapy context, TEs and NTEs can be involved at the same time, and in the case of NTEs, they could present several risks of complications when the irradiated area is very close to a sensitive organ. On the other hand, NTEs could increase the biological effect of the radiotherapy on distant non-irradiated cancer cells (such as metastases) with immune-associated effects (Abscopal effect) or on non-irradiated cancer cells adjacent to cancer cells specifically targeted with radioactive antibodies (positive Bystander effect).

I am pleased to invite you to participate in this Special Issue, "Targeted and non-targeted effects of ionizing radiation in a context of cancer radiotherapy". Research papers, up-to-date review articles, and commentaries are all welcome.

Dr. François Chevalier
Guest Editor

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Keywords

  • non-targeted effects
  • radiation-induced bystander effect
  • abscopal effect
  • genomic instability
  • low dose effects
  • radioprotection
  • circulating biomarkers
  • oxidative stress

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Published Papers (1 paper)

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Research

24 pages, 17138 KiB  
Article
Single-Cell Sequencing Reveals the Role of Radiation-Induced Stemness-Responsive Cancer Cells in the Development of Radioresistance
by Zheng Shi, Cuilan Hu, Jiadi Liu, Wei Cheng, Xiaohua Chen, Xiongxiong Liu, Yanyu Bao, Haidong Tian, Boyi Yu, Feifei Gao, Fei Ye, Xiaodong Jin, Chao Sun and Qiang Li
Int. J. Mol. Sci. 2025, 26(4), 1433; https://doi.org/10.3390/ijms26041433 - 8 Feb 2025
Viewed by 830
Abstract
Increased stemness of cancer cells exacerbates radioresistance, thereby greatly limiting the efficacy of radiotherapy. In order to study the changes in cancer cell stemness during radiotherapy, we established a radioresistance model of human non-small cell lung cancer A549 cells and obtained A549 radioresistant [...] Read more.
Increased stemness of cancer cells exacerbates radioresistance, thereby greatly limiting the efficacy of radiotherapy. In order to study the changes in cancer cell stemness during radiotherapy, we established a radioresistance model of human non-small cell lung cancer A549 cells and obtained A549 radioresistant cells (A549-RR). We sampled the cells at different time points during the modeling process and investigated the heterogeneity of each group of cells using single-cell sequencing. Cells in the early stages of fractionated irradiation were found to be significantly up-regulated in stemness, and a subpopulation of cells producing this response was screened and referred to as “radiation-induced stemness-responsive cancer cells”. They were undergoing stemness response, energy metabolism reprogramming, and progressively differentiating into cells with more diverse and malignant phenotypes in order to attenuate the killing effect of radiation. Furthermore, we demonstrated that such responses might be driven by the activation of the EGFR-Hippo signaling pathway axis, which also plays a crucial role in the development of radioresistance. Our study reveals the dynamic evolution of cell subpopulation in cancer cells during fractionated radiotherapy; the early stage of irradiation can determine the destiny of the radiation-induced stemness-responsive cancer cells. The activation of stemness-like phenotypes during the development of radioresistance is not the result of dose accumulation but occurs during the early stage of radiotherapy with relatively low-dose irradiation. The degree of the radiation-induced stemness response of cancer cells mediated by the EGFR-Hippo signaling pathway might be a potential predictor of the efficacy of radiotherapy and the development of radioresistance. Full article
(This article belongs to the Special Issue Effects of Ionizing Radiation in Cancer Radiotherapy: 2nd Edition)
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