ArticleRadiation oncology (London, England)2015
VE-821, an ATR inhibitor, causes radiosensitization in human tumor cells irradiated with high LET radiation.
Article in Radiation oncology (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Transient ATR inhibition following ionizing radiation enhances immune-mediated antitumor response and survival.bioRxiv : the preprint server for biology · 2026Article
- O-GlcNAcylation of NONO mediates alternative splicing of SETMAR and facilitates NHEJ repair.Genome biology · 2026Article
- Development of Prognostic Features and Investigation of Therapeutic Insights Related to Non-Apoptotic Regulatory Cell Death in Colorectal Cancer.Applied biochemistry and biotechnology · 2025Article
- ATR inhibition radiosensitizes cells through augmented DNA damage and G2 cell cycle arrest abrogation.JCI insight · 2024Article
- Potential Benefits of Combining Proton or Carbon Ion Therapy with DNA Damage Repair Inhibitors.Cells · 2024Review
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- Synergistic Activity of DNA Damage Response Inhibitors in Combination with Radium-223 in Prostate Cancer.Cancers · 2024Article
- Key molecular DNA damage responses of human cells to radiation.Frontiers in cell and developmental biology · 2024Review
- Intra-promoter switch of transcription initiation sites in proliferation signaling-dependent RNA metabolism.Nature structural & molecular biology · 2023Article
- DNA damage and repair dependencies of ionising radiation modalities.Bioscience reports · 2023Review
- Invalidity of, and alternative to, the linear quadratic model as a predictive model for postirradiation cell survival.Cancer science · 2023Article
- The ATR Inhibitor VE-821 Enhances the Radiosensitivity and Suppresses DNA Repair Mechanisms of Human Chondrosarcoma Cells.International journal of molecular sciences · 2023Article
- DNA Damage Response in Cancer Therapy and Resistance: Challenges and Opportunities.International journal of molecular sciences · 2022Review
- Bioprospecting the microbiome of Red Sea Atlantis II brine pool for peptidases and biosynthetic genes with promising antibacterial activity.Microbial cell factories · 2022Article
- Recent Advances in Synergistic Antitumor Effects Exploited from the Inhibition of Ataxia Telangiectasia and RAD3-Related Protein Kinase (ATR).Molecules (Basel, Switzerland) · 2022Review
- DNA Damage Clustering after Ionizing Radiation and Consequences in the Processing of Chromatin Breaks.Molecules (Basel, Switzerland) · 2022Review
- Strong Shift to ATR-Dependent Regulation of the GLife (Basel, Switzerland) · 2021Article
- DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer.Signal transduction and targeted therapy · 2020Review
- Overcoming radioresistance in WiDr cells with heavy ion irradiation and radiosensitization by 2-deoxyglucose with photon irradiation.Clinical and translational radiation oncology · 2019Article
- Antibacterial and anticancer activities of orphan biosynthetic gene clusters from Atlantis II Red Sea brine pool.Microbial cell factories · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh linear energy transfer (LET) radiation such as carbon ion particles is successfully used for treatment of solid tumors. The reason why high LET radiation accomplishes greater tumor-killing than X-rays is still not completely understood. One factor would be the clustered or complex-type DNA damages. We previously reported that complex DNA double-strand breaks produced by high LET radiation enhanced DNA end resection, and this could lead to higher kinase activity of ATR protein recruited to RPA-coated single-stranded DNA. Although the effect of ATR inhibition on cells exposed to low LET gamma-rays has recently been reported, little is known regarding the effect of ATR inhibitor on cells treated with high LET radiation. The purpose of this study is to investigate the effects of the ATR inhibitor VE-821 in human tumor and normal cells irradiated with high LET carbon ions.
findingsHeLa, U2OS, and 1BR-hTERT (normal) cells were pre-treated with 1 μM VE-821 for 1 hour and irradiated with either high LET carbon ions or X-rays. Cell survival, cell cycle distribution, cell growth, and micronuclei formation were evaluated. VE-821 caused abrogation of G2/M checkpoint and forced irradiated cells to divide into daughter cells. We also found that carbon ions caused a higher number of multiple micronuclei than X-rays, leading to decreased cell survival in tumor cells when treated with VE-821, while the survival of irradiated normal cells were not significantly affected by this inhibitor.
conclusionsATR inhibitor would be an effective tumor radiosensitizer with carbon ion irradiation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.