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Molecular Insights into Radiation Oncology

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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 (30 November 2025) | Viewed by 12676

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Special Issue Editor

Prof. Dr. Allen Chen

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Guest Editor

Department of Radiation Oncology, University of California, Irvine, CA 92868, USA
Interests: radiation; head and neck cancers; HPV; re-irradiation techniques; oncology

Special Issue Information

Dear Colleagues,

Radiation therapy or radiotherapy is a treatment using ionizing radiation that is generally provided as part of cancer therapy to either kill or control the growth of malignant cells. Radiation therapy works by damaging the DNA of cancer cells and can cause them to undergo mitotic catastrophe. However, radiation affects normal cells as well as cancerous cells, causing side effects in the treatment area.

In this Special Issue, we aim to comprehensively dissect the molecular mechanisms by which radiation therapy influences the initiation and progression of tumors. In addition, we would like to advance the development of cancer treatments that target the mechanisms of radiation therapy and reduce the side effects of radiation. We invite submissions of original research articles and comprehensive reviews that can help to advance our molecular understanding of radiation oncology. Subtopics may include, but are not limited to, the following:

Molecular mechanisms in radiation oncology;
Developing new drugs that target the mechanisms by which radiation affects tumor initiation and progression;
Reducing side effects from radiation and the mechanisms behind them;

• Exploring personalized treatment options related to radiation oncology.

Prof. Dr. Allen M. Chen
Guest Editor

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Keywords

molecular and cellular radiobiology
radiation physics
DNA damage and repair
radiation response
cancers

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Published Papers (8 papers)

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Research

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16 pages, 397 KB

Open AccessArticle

NGAL and HPV Subtypes in Cervical Carcinoma: Implications for Cancer Progression and Treatment Response

by Behar Raci, Snezana Stojkovska, Gezim Hodolli, Violeta Klisarovska, Goran Dimitrov, Shemsi Veseli, Arta Kameri-Jusufi, Mentor Kurshumliu, Diellor Rizaj and Arben Sinani

Curr. Issues Mol. Biol. 2026, 48(2), 234; https://doi.org/10.3390/cimb48020234 - 23 Feb 2026

Viewed by 439

Abstract

Background/Objectives: Cervical cancer is a prominent source of morbidity and mortality among women, particularly in low- and middle-income nations. Neutrophil Gelatinase-Associated Lipocalin (NGAL), a glycoprotein involved in cancer-related activities, has been proposed as a biomarker; however, its involvement in cervical cancer remains unknown. The study aim is to evaluate the prognostic significance of serum NGAL levels in cervical cancer patients in relation to International Federation of Gynecology and Obstetrics (FIGO) stage, operability, and HPV subtype distribution before and after treatment. Methods: The study involved 130 women, 100 with histologically proven cervical cancer and 30 healthy controls. The serum NGAL levels were determined before and after treatment using an ELISA test. HPV genotyping was carried out using real-time PCR on 21 high- and low-risk subtypes. Results: NGAL levels increased marginally during therapy (from 134 to 144 ng/mL; p = 0.28), but the rise was significant in inoperable patients (p = 0.02) and increased with advanced FIGO stage, although this did not reach statistical significance (p = 0.07). HPV 16 was the most common subtype (26.0%), while women aged 51–60 had the highest overall HPV positive rate (72.7%). There was no significant association between NGAL levels and HPV subtypes (p = 0.17). Conclusion: NGAL does not appear to be an accurate short-term indicator of therapy response. However, increased levels in advanced-stage and inoperable instances indicate prognostic significance. NGAL most likely represents tumor-associated inflammation rather than HPV subtype. These findings support its possible inclusion in future biomarker panels, subject to validation in bigger investigations. Persistent HPV infection in midlife women highlights the significance of ongoing screening. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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14 pages, 4195 KB

Open AccessArticle

Role of the Super-Enhancer Component Bromodomain Protein 4 in the Radiation Response of Human Head and Neck Squamous Cell Carcinoma Cells

by Nanami Munakata, Hironori Yoshino, Masaharu Hazawa and Eichi Tsuruga

Curr. Issues Mol. Biol. 2026, 48(1), 71; https://doi.org/10.3390/cimb48010071 - 10 Jan 2026

Viewed by 598

Abstract

Radiotherapy is an effective treatment for cancer; however, radioresistant cancer cells result in recurrence. Therefore, elucidating the mechanisms of radioresistance is urgently needed. Super-enhancers (SEs) are clusters of enhancers occupied by a high density of master transcription factors, mediators, and bromodomain protein BRD4. Recently, we reported that ΔNp63, an oncogenic transcription factor, promotes radioresistance in human head and neck squamous cell carcinoma (HNSCC) cells. As ΔNp63 establishes SEs in HNSCC cells, SEs may be involved in radioresistance. Here, we investigated the role of the SE component BRD4 in the radiation responses of HNSCC cells using a BRD4 degrader ARV-771 or BRD4 knockdown. First, Western blotting confirmed that ARV-771 decreased BRD4 protein expression. ARV-771 treatment resulted in reduced cell proliferation and enhanced apoptosis in irradiated HNSCC cells. Moreover, colony formation assays revealed that both ARV-771 and BRD4 knockdown enhanced the radiosensitivity of HNSCC cells, suggesting BRD4 contributes to the radioresistance of HNSCC cells. Furthermore, fluorescence immunostaining revealed distinct localization patterns of γH2AX, a marker of DNA double-strand breaks, compared with BRD4 and ΔNp63 in irradiated cells. Notably, ARV-771 and BRD4 knockdown decreased ΔNp63 and BRD4 protein expression, whereas ΔNp63 knockdown had minimal impact on BRD4 expression. Taken together, these findings suggest that BRD4-dependent maintenance of ΔNp63 expression may contribute, at least in part, to the regulation of radioresistance in HNSCC cells. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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19 pages, 5171 KB

Open AccessEditor’s ChoiceArticle

Interferon-Type-I Response and Autophagy Independently Regulate Radiation-Induced HLA-Class-I Molecule Expression in Lung Cancer

by Erasmia T. Xanthopoulou, Ioannis Lamprou, Ioannis M. Koukourakis, Achilleas G. Mitrakas, Georgios D. Michos, Anastasia Polyzoidou, Filippos G. Antoniadis, Alexandra Giatromanolaki and Michael I. Koukourakis

Curr. Issues Mol. Biol. 2026, 48(1), 28; https://doi.org/10.3390/cimb48010028 - 25 Dec 2025

Viewed by 649

Abstract

Background/Objectives: The enhancement of antitumor immune responses by radiotherapy (RT) is partially attributed to the activation of the IFN-type-I pathway. However, the loss of HLA-class-I molecules, which occurs in a large percentage of non-small-cell lung cancers (NSCLCs), may block the cytotoxic effect of T-cells and immunotherapy (IO). Moreover, autophagy is also involved in HLA downregulation. We investigated the complex interactions between RT, HLA molecules, autophagy, and IFN-type-I responses. Methods: The A549, H1299, and ATG7-deficient NSCLC cell lines, along with the modified shLC3A H1299 cell line, were used for in vitro experiments. The effect of RT (8 and 3 × 8 Gy) on Interferon beta (IFNβ), IFN-stimulated genes (ISGs), and HLA-class-I expression in combination with IFN-type-I-response inhibitors (Ruxolitinib, Tofacitinib, Amlexanox) targeting the JAK and TBK1 was studied with Flow cytometry and RT-PCR. Results: RT significantly induced HLA-class-I expression. A parallel upregulation of IFNβ and ISGs mRNA levels was also documented. Although the IFN-type-I-response inhibitors suppressed the RT-induced IFNβ and ISGs expression, their effect on HLA-class-I expression was minimal. Blockage of LC3A autophagy (shLC3A cell line) significantly upregulated HLA-class-I basal levels, and RT further enhanced HLA expression. IFN-type-I-response inhibitors blocked the RT-inductive effect in the shLC3A H1299, but had no effect in the ATG7-deficient H1650 cell line. Conclusions: The current study supports the theory that baseline autophagy, RT-induced autophagy blockage, and IFN-type-I response enhancement define the HLA-class-I levels in NSCLC cells. This complex interplay emerges as a promising target for the development of radio-vaccination strategies to enhance the efficacy of radio-immunotherapy. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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16 pages, 4440 KB

Open AccessArticle

Action of Carnosic Acid Against Melanoma: A Strategy for Selective Radiosensitization with Protection of Non-Tumoral Cells

by Amparo Olivares, Isabel de la Fuente, Daniel Gyingiri Achel, Ana María Mercado, José Antonio Garcia-Gamuz, María del Rosario Tudela and Miguel Alcaraz

Curr. Issues Mol. Biol. 2025, 47(10), 845; https://doi.org/10.3390/cimb47100845 - 14 Oct 2025

Viewed by 818

Abstract

Carnosic acid (CA) is a phenolic diterpene with high antioxidant activity that supports its radioprotective capacity. This study aims to determine whether the radiosensitizing effect of CA established in B16F10 melanoma cells also occurs in other melanin-producing cells. Cell survival analysis, apoptosis, intracellular glutathione levels, and cell cycle progression were evaluated by comparing radiosensitive cells (PNT2) with radioresistant melanin-producing cells (MELAN A, SK-MEL-1, and B16F10). In PNT2 cells, CA exhibited radioprotective capacity, with 100% cell survival after exposure to 20 Gy of X-rays (p < 0.001), decreasing apoptosis (p < 0.001) and increasing the GSH/GSSG ratio (p < 0.01), without significant modification in cell cycle progression. However, CA administration to irradiated cells failed to exert radioprotection in MELAN A and SK-MEL-1 cells, and even doubled cell death in B16F10 cells (p < 0.001). Specifically, CA did not alter apoptosis or prevent the decrease in GSH/GSSG ratio in MELAN A and SK-MEL-1 cells, while it intensified radiation-induced cell cycle disruptions in all melanin-producing cells. All of these led to a loss of radioprotective capacity in the melanin-producing cells (MELAN A and SK-MEL-1) and even induced a radiosensitizing effect in B16F10 cells. Understanding the mechanisms of action of substances such as CA could promote new applications that protect healthy cells and exclusively damage neoplastic cells when both are present within the same irradiated volume in cancer patients requiring radiotherapy. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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11 pages, 756 KB

Open AccessArticle

Investigating LATS1 and NF-κB as Predictors of Radiotherapy Response in Cervical Cancer

by Andi Darma Putra, Andrijono, Hariyono Winarto, Ani Retno Prijanti, Lisnawati, Trevino Aristarkus Pakasi, Supriadi Gandamihardja, Jourdan Wirasugianto, Amelia and Lasmini Syariatin

Curr. Issues Mol. Biol. 2025, 47(5), 365; https://doi.org/10.3390/cimb47050365 - 16 May 2025

Cited by 1 | Viewed by 1301

Abstract

Cervical cancer is the fourth most prevalent cancer among women globally. Protein concentrations of Large Tumor Suppressor Kinase-1 (LATS1) and Nuclear Factor Kappa-B (NF-κB) have been identified as prospective biomarkers of radioresistance in cervical cancer. This preliminary study aimed to investigate the effectiveness of LATS1 and NF-κB levels as a biomarker for radioresistance and evaluate their response to radiation in cervical cancer patients. A comprehensive cross-sectional study was conducted involving 114 subjects diagnosed with advanced stages cervical cancer (stage IIIB and IVA) who underwent definitive radiotherapy. The concentrations of LATS1 and NF-κB were measured using ELISA from biopsy samples taken prior to the initiation of radiotherapy. This study’s finding included 114 subjects, with a median age of 53 years. A total of 85 (74.5%) subjects had stage IIIB, while 29 (25.4%) subjects had stage IVA. The cut-offs for LATS1 and NF-κB were 0.02765 ng/mg and 192.42 pg/mg, respectively. Subjects with a higher expression of LATS1 were found to be unresponsive to radiation therapy (p ≤ 0.001; AUC = 32.7%), and subjects with a lower expression of NF-κB were found to be unresponsive to radiation therapy (p = 0.009; AUC = 61%). This study suggests that elevated LATS1 expression may inversely predict radioresistance, while NF-κB expression shows a weak correlation with resistance to radiation therapy. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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21 pages, 3935 KB

Open AccessArticle

The Dose Rate of Corpuscular Ionizing Radiation Strongly Influences the Severity of DNA Damage, Cell Cycle Progression and Cellular Senescence in Human Epidermoid Carcinoma Cells

by Sergey S. Soroko, Dmitry V. Skamnitskiy, Ekaterina N. Gorshkova, Olga M. Kutova, Ismail R. Seriev, Anna V. Maslennikova, Evgeniy L. Guryev, Sergey V. Gudkov, Vladimir A. Vodeneev, Irina V. Balalaeva and Natalia Yu Shilyagina

Curr. Issues Mol. Biol. 2024, 46(12), 13860-13880; https://doi.org/10.3390/cimb46120828 - 6 Dec 2024

Cited by 4 | Viewed by 3376

Abstract

Modern radiotherapy utilizes a broad range of sources of ionizing radiation, both low-dose-rate (LDR) and high-dose-rate (HDR). However, the mechanisms underlying specific dose-rate effects remain unclear, especially for corpuscular radiation. To address this issue, we have irradiated human epidermoid carcinoma A431 cells under LDR and HDR regimes. Reducing the dose rate has lower lethality at equal doses with HDR irradiation. The half-lethal dose after HDR irradiation was three times less than after LDR irradiation. The study of mechanisms showed that under HDR irradiation, the radiation-induced halt of mitosis with the accompanying emergence of giant cells was recorded. No such changes were recorded after LDR irradiation. The level of DNA damage is significantly greater after HDR irradiation, which may be the main reason for the different mechanisms of action of HDR and LDR irradiations. Comparing the mechanisms of cell response to LDR and HDR irradiations may shed light on the mechanisms of tumor cell response to ionizing radiation and answer the question of whether different dose rates within the same dose range can cause different clinical effects. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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16 pages, 1940 KB

Open AccessArticle

Preliminary Study on Lutetium-177 and Gold Nanoparticles: Apoptosis and Radiation Enhancement in Hepatic Cancer Cell Line

by Maria Anthi Kouri, Anastasios Georgopoulos, George E. Manios, Eirini Maratou, Aris Spathis, Sofia Chatziioannou, Kalliopi Platoni and Efstathios P. Efstathopoulos

Curr. Issues Mol. Biol. 2024, 46(11), 12244-12259; https://doi.org/10.3390/cimb46110727 - 30 Oct 2024

Cited by 5 | Viewed by 2496

Abstract

This study investigates a novel approach toward enhancing the efficacy of Lutetium-177 (Lu-177) radiopharmaceutical therapy by combining it with gold nanoparticles (AuNPs) in the HepG2 hepatic cancer cell line. Lu-177, known for its effective β radiation, also emits gamma rays at energies (113 keV and 208 keV) near the photoelectric absorption range, suggesting potential for targeted and localized radiation enhancement when used in conjunction with AuNPs. Thus, HepG2 cells were treated at two different activity levels (74 MBq and 148 MBq), with Lu-177 alone, with a combination of Lu-177 and AuNPs in two sizes (10 nm and 50 nm), while some received no treatment. Treatment efficacy was assessed by quantifying the radiation enhancement ratio (RER) and the apoptosis levels. The results reveal that combining Lu-177 with AuNPs significantly increases cell death and apoptosis compared to Lu-177 alone, with 10 nm AuNPs demonstrating superior effectiveness. Additionally, varying Lu-177 activity levels influenced the treatment outcomes, with higher activity levels further augmenting the therapeutic impact of combined therapy. These findings underscore the potential of utilizing Lu-177’s beta, but also gamma, emissions, traditionally considered non-therapeutic, for localized radiation enhancement when combined with AuNPs. This novel strategy leverages Lu-177 as an internal irradiator to exploit gamma radiation for a targeted therapeutic advantage without requiring nanoparticle functionalization. The study provides a promising approach to improving radionuclide therapy and sets the stage for future research aimed at optimizing cancer treatments through the combined use of Lu-177 and AuNPs. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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Review

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18 pages, 2590 KB

Open AccessReview

Prophylactic Cranial Irradiation in Small Cell Lung Cancer: Evolution of Evidence, Current Status, and Future Directions

by Swati Mamidanna, Menal Bhandari, Charvi Shah, Ludvinna Bazile, Sukhdeep Kaur Gill, Adeel Riaz, Lakshmi Rekha Narra, Shreel Parikh, Ahmed Shalaby, Mihir Patel, Zohaib Khan Sherwani, Jongmyung Kim, Matthew P. Deek, Salma K. Jabbour and Ritesh Kumar

Curr. Issues Mol. Biol. 2025, 47(12), 998; https://doi.org/10.3390/cimb47120998 - 28 Nov 2025

Viewed by 2181

Abstract

Small cell lung cancer (SCLC) is an aggressive malignancy with a high incidence of brain metastases. Prophylactic cranial irradiation (PCI) was developed to reduce central nervous system (CNS) relapses and has been shown to improve survival, particularly in limited-stage disease. The pivotal Auperin meta-analysis and subsequent studies confirmed its role in patients achieving a complete response to initial therapy. In extensive-stage SCLC, earlier trials demonstrated reduced brain metastases and modest survival gains, but more recent studies incorporating routine magnetic resonance imaging (MRI) surveillance failed to show overall survival benefits, supporting MRI monitoring with salvage therapy as an alternative. Neurocognitive toxicity remains the major limitation of PCI, especially in older adults. Common effects include memory impairment, cognitive changes, and a reduced quality of life. Advances such as hippocampal avoidance PCI and neuroprotective strategies like memantine have shown the ability to mitigate long-term decline. Modern radiotherapy techniques, including intensity modulated radiation therapy (IMRT) and volumetric modulated arc therapy (VMAT), enable the precise sparing of critical structures while maintaining intracranial control. The integration of immunotherapy has shifted treatment paradigms in SCLC. While checkpoint inhibitors have improved systemic outcomes, their impact on brain relapses and interactions with PCI remain uncertain. This review provides an overview of the evolution of PCI in SCLC, while emphasizing current challenges and future directions. Full article

(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)

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