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Understanding Cellular Radiation Responses for Radiation Therapy
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Understanding Cellular Radiation Responses for Radiation Therapy

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 8341

Special Issue Editor

Dr. Hironori Yoshino

E-Mail Website
Guest Editor
Department of Radiation Science, Graduate School of Health Sciences, Hirosaki University, Hirosaki 036-8564, Aomori, Japan
Interests: radiation; apoptosis; mitochondria; anticancer drug; innate immunity; antitumor immunity; radiosensitization

Special Issue Information

Dear Colleagues,

Radiation therapy is one of the major treatments for cancer; however, there are some issues, such as the existence of cancer cells that show resistance to radiation as well as the side effects that occur in normal cells and tissues. Therefore, it is necessary to understand the radiation responses of normal and cancer cells.

This Special Issue of Current Issues in Molecular Biology will focus on the cellular radiation responses of both normal and cancer cells. I am widely recruiting original research articles and review articles that improve our understanding of cellular radiation responses for cancer therapy. For example, I welcome articles that clarify the mechanisms that regulate the resistance of cancer cells to radiation (such as molecular targets) and that describe strategies with which to overcome it. In addition, I welcome articles that show pharmaceutical drugs that relieve radiation-induced cytotoxicity. 

Dr. Hironori Yoshino
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • radiation therapy
  • radioresistance
  • radiosensitization
  • radiosensitizer
  • radioprotector
  • radiation mitigator

Published Papers (6 papers)

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Research

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12 pages, 3221 KiB  
Article
Hyperbaric Oxygen Therapy Adjuvant Chemotherapy and Radiotherapy through Inhibiting Stemness in Glioblastoma
by Chun-Man Yuen, Hung-Pei Tsai, Tzu-Ting Tseng, Yu-Lung Tseng, Ann-Shung Lieu, Aij-Lie Kwan and Alice Y. W. Chang
Curr. Issues Mol. Biol. 2023, 45(10), 8309-8320; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45100524 - 12 Oct 2023
Viewed by 1938
Abstract
Glioblastoma multiforme (GBM) is the most common and deadliest primary brain tumor in adults. Despite the advances in GBM treatment, outcomes remain poor, with a 2-year survival rate of less than 5%. Hyperbaric oxygen (HBO) therapy is an intermittent, high-concentration, short-term oxygen therapy [...] Read more.
Glioblastoma multiforme (GBM) is the most common and deadliest primary brain tumor in adults. Despite the advances in GBM treatment, outcomes remain poor, with a 2-year survival rate of less than 5%. Hyperbaric oxygen (HBO) therapy is an intermittent, high-concentration, short-term oxygen therapy used to increase cellular oxygen content. In this study, we evaluated the effects of HBO therapy, alone or combined with other treatment modalities, on GBM in vitro and in vivo. In the in vitro analysis, we used a 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to assess the effects of HBO therapy alone, a colony formation assay to analyze the effects of HBO therapy combined with radiotherapy and with temozolomide (TMZ), and a neurosphere assay to assess GBM stemness. In the in vivo analysis, we used immunohistochemical staining and in vivo bioluminescence imaging to assess GBM stemness and the therapeutic effect of HBO therapy alone or combined with TMZ or radiotherapy, respectively. HBO therapy did not affect GBM cell viability, but it did reduce the analyzed tumors’ ability to form cancer stem cells. In addition, HBO therapy increased GBM sensitivity to TMZ and radiotherapy both in vitro and in vivo. HBO therapy did not enhance tumor growth and exhibited adjuvant effects to chemotherapy and radiotherapy through inhibiting GBM stemness. In conclusion, HBO therapy shows promise as an adjuvant treatment for GBM by reducing cancer stem cell formation and enhancing sensitivity to chemotherapy and radiotherapy. Full article
(This article belongs to the Special Issue Understanding Cellular Radiation Responses for Radiation Therapy)
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22 pages, 2982 KiB  
Article
Dose-Dependent Shift in Relative Contribution of Homologous Recombination to DNA Repair after Low-LET Ionizing Radiation Exposure: Empirical Evidence and Numerical Simulation
by Oleg Belov, Anna Chigasova, Margarita Pustovalova, Andrey Osipov, Petr Eremin, Natalia Vorobyeva and Andreyan N. Osipov
Curr. Issues Mol. Biol. 2023, 45(9), 7352-7373; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45090465 - 9 Sep 2023
Cited by 1 | Viewed by 938
Abstract
Understanding the relative contributions of different repair pathways to radiation-induced DNA damage responses remains a challenging issue in terms of studying the radiation injury endpoints. The comparative manifestation of homologous recombination (HR) after irradiation with different doses greatly determines the overall effectiveness of [...] Read more.
Understanding the relative contributions of different repair pathways to radiation-induced DNA damage responses remains a challenging issue in terms of studying the radiation injury endpoints. The comparative manifestation of homologous recombination (HR) after irradiation with different doses greatly determines the overall effectiveness of recovery in a dividing cell after irradiation, since HR is an error-free mechanism intended to perform the repair of DNA double-strand breaks (DSB) during S/G2 phases of the cell cycle. In this article, we present experimentally observed evidence of dose-dependent shifts in the relative contributions of HR in human fibroblasts after X-ray exposure at doses in the range 20–1000 mGy, which is also supported by quantitative modeling of DNA DSB repair. Our findings indicate that the increase in the radiation dose leads to a dose-dependent decrease in the relative contribution of HR in the entire repair process. Full article
(This article belongs to the Special Issue Understanding Cellular Radiation Responses for Radiation Therapy)
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9 pages, 1785 KiB  
Communication
Dose Rate Effect on Cell Survival in BNCT
by Katsumi Hirose, Mariko Sato, Koji Ichise and Masahiko Aoki
Curr. Issues Mol. Biol. 2023, 45(9), 6986-6994; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45090441 - 23 Aug 2023
Viewed by 1293
Abstract
The output constancy of the accelerator used for boron neutron capture therapy (BNCT) is essential to ensuring anti-tumor efficacy and safety. BNCT as currently practiced requires a wide variety of beam quality assessments to ensure that RBE dose errors are maintained within 5%. [...] Read more.
The output constancy of the accelerator used for boron neutron capture therapy (BNCT) is essential to ensuring anti-tumor efficacy and safety. BNCT as currently practiced requires a wide variety of beam quality assessments to ensure that RBE dose errors are maintained within 5%. However, the necessity of maintaining a constant beam dose rate has not been fully discussed. We therefore clarified the effect of different physical dose rates of the accelerator BNCT on biological effects. SAS and A172 cells exposed to 10B-boronophenylalanine were irradiated using a neutron beam (normal operating current, 100 μA) at the Aomori Quantum Science Center. Thermal neutron flux was attenuated to 50.0 ± 0.96% under 50 μA irradiation compared to that under 100 μA irradiation. Cells were given physical doses of 1.67 and 3.36 Gy at 30 and 60 mC, respectively, and survival was significantly increased after 50 μA irradiation for both cell types (p = 0.0052 for SAS; p = 0.046 for A172, for 60 mC). Differences in accelerator BNCT beam dose rates have non-negligible effects on biological effects. Dose rate fluctuations and differences should not be easily permitted to obtain consistent biological effects. Full article
(This article belongs to the Special Issue Understanding Cellular Radiation Responses for Radiation Therapy)
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10 pages, 3164 KiB  
Communication
ΔNp63 Regulates Radioresistance in Human Head and Neck Squamous Carcinoma Cells
by Kota Sato, Hironori Yoshino, Yoshiaki Sato, Manabu Nakano and Eichi Tsuruga
Curr. Issues Mol. Biol. 2023, 45(8), 6262-6271; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45080394 - 27 Jul 2023
Viewed by 1052
Abstract
Radiation therapy is commonly used to treat head and neck squamous cell carcinoma (HNSCC); however, recurrence results from the development of radioresistant cancer cells. Therefore, it is necessary to identify the underlying mechanisms of radioresistance in HNSCC. Previously, we showed that the inhibition [...] Read more.
Radiation therapy is commonly used to treat head and neck squamous cell carcinoma (HNSCC); however, recurrence results from the development of radioresistant cancer cells. Therefore, it is necessary to identify the underlying mechanisms of radioresistance in HNSCC. Previously, we showed that the inhibition of karyopherin-β1 (KPNB1), a factor in the nuclear transport system, enhances radiation-induced cytotoxicity, specifically in HNSCC cells, and decreases the localization of SCC-specific transcription factor ΔNp63. This suggests that ΔNp63 may be a KPNB1-carrying nucleoprotein that regulates radioresistance in HNSCC. Here, we determined whether ΔNp63 is involved in the radioresistance of HNSCC cells. Cell survival was measured by a colony formation assay. Apoptosis was assessed by annexin V staining and cleaved caspase-3 expression. The results indicate that ΔNp63 knockdown decreased the survival of irradiated HNSCC cells, increased radiation-induced annexin V+ cells, and cleaved caspase-3 expression. These results show that ΔNp63 is involved in the radioresistance of HNSCC cells. We further investigated which specific karyopherin-α (KPNA) molecules, partners of KPNB1 for nuclear transport, are involved in nuclear ΔNp63 expression. The analysis of nuclear ΔNp63 protein expression suggests that KPNA1 is involved in nuclear ΔNp63 expression. Taken together, our results suggest that ΔNp63 is a KPNB1-carrying nucleoprotein that regulates radioresistance in HNSCC. Full article
(This article belongs to the Special Issue Understanding Cellular Radiation Responses for Radiation Therapy)
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11 pages, 6100 KiB  
Article
Edaravone Exerts Protective Effects on Mice Intestinal Injury without Interfering with the Anti-Tumor Effects of Radiation
by Terufumi Kawamoto and Keisuke Sasai
Curr. Issues Mol. Biol. 2023, 45(7), 5362-5372; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45070340 - 28 Jun 2023
Cited by 1 | Viewed by 1104
Abstract
The appropriate dosage of edaravone—a radioprotective agent—and its effect on tumors are unknown. This study evaluated the effects of edaravone on intestinal injuries and tumors in mice induced by whole body X-ray irradiation. Small intestinal mucositis was induced in C3H/HeNSlc mice using a [...] Read more.
The appropriate dosage of edaravone—a radioprotective agent—and its effect on tumors are unknown. This study evaluated the effects of edaravone on intestinal injuries and tumors in mice induced by whole body X-ray irradiation. Small intestinal mucositis was induced in C3H/HeNSlc mice using a single X-ray dose (15 Gy). Edaravone (15, 30, and 100 mg/kg) was administered 30 min before irradiation to evaluate its protective effect. After 3.5 days, the jejunum was removed and the histological changes were evaluated. Next, C3H/HeNSlc mice with squamous cell carcinoma VII tumors were provided the same single X-ray dose and 100 mg/kg edaravone; further, the tumors were immediately induced after irradiation. The tumor cell viability was detected using an in vivo–in vitro colony formation assay. We found that the intestinal colony-forming ability after irradiation was significantly higher in the 100 mg/kg edaravone group than that in the control group. Moreover, the apoptotic cells in the villi immunohistochemically stained with cleaved caspase-3 were significantly lower in the 100 mg/kg edaravone group than in the control group. We found no radioprotective effects of intraperitoneally inoculated edaravone in both hind legs on squamous cell carcinoma VII tumors. These findings suggest that 100 mg/kg edaravone exerts protective effects on small intestinal injuries without interfering with the antitumor effects of radiation. Full article
(This article belongs to the Special Issue Understanding Cellular Radiation Responses for Radiation Therapy)
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Review

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23 pages, 433 KiB  
Review
Immune Response and Immune Checkpoint Molecules in Patients with Rectal Cancer Undergoing Neoadjuvant Chemoradiotherapy: A Review
by Ioannis M. Koukourakis, Kalliopi Platoni, Dina Tiniakos, Vassilis Kouloulias and Anna Zygogianni
Curr. Issues Mol. Biol. 2023, 45(5), 4495-4517; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45050285 - 22 May 2023
Cited by 1 | Viewed by 1429
Abstract
It is well-established that tumor antigens and molecules expressed and secreted by cancer cells trigger innate and adaptive immune responses. These two types of anti-tumor immunity lead to the infiltration of the tumor’s microenvironment by immune cells with either regulatory or cytotoxic properties. [...] Read more.
It is well-established that tumor antigens and molecules expressed and secreted by cancer cells trigger innate and adaptive immune responses. These two types of anti-tumor immunity lead to the infiltration of the tumor’s microenvironment by immune cells with either regulatory or cytotoxic properties. Whether this response is associated with tumor eradication after radiotherapy and chemotherapy or regrowth has been a matter of extensive research through the years, mainly focusing on tumor-infiltrating lymphocytes and monocytes and their subtypes, and the expression of immune checkpoint and other immune-related molecules by both immune and cancer cells in the tumor microenvironment. A literature search has been conducted on studies dealing with the immune response in patients with rectal cancer treated with neoadjuvant radiotherapy or chemoradiotherapy, assessing its impact on locoregional control and survival and underlying the potential role of immunotherapy in the treatment of this cancer subtype. Here, we provide an overview of the interactions between local/systemic anti-tumor immunity, cancer-related immune checkpoint, and other immunological pathways and radiotherapy, and how these affect the prognosis of rectal cancer patients. Chemoradiotherapy induces critical immunological changes in the tumor microenvironment and cancer cells that can be exploited for therapeutic interventions in rectal cancer. Full article
(This article belongs to the Special Issue Understanding Cellular Radiation Responses for Radiation Therapy)
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