ArticleRadiation and environmental biophysics2013
Inhibition of ATR kinase with the selective inhibitor VE-821 results in radiosensitization of cells of promyelocytic leukaemia (HL-60).
Article in Radiation and environmental biophysics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 32 citations in OpenAlex.
- The CHK1 inhibitor Prexasertib is effective againstFrontiers in endocrinology · 2026Article
- Novel Cellular Functions of ATR for Therapeutic Targeting: Embryogenesis to Tumorigenesis.International journal of molecular sciences · 2023Review
- Selective vulnerability of ARID1A deficient colon cancer cells to combined radiation and ATR-inhibitor therapy.Frontiers in oncology · 2022Article
- Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment.Experimental hematology & oncology · 2021Review
- ATR/CHK1 inhibitors and cancer therapy.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2018Review
- Article
- The cell cycle checkpoint inhibitors in the treatment of leukemias.Journal of hematology & oncology · 2017Review
- IGF-1R inhibition sensitizes breast cancer cells to ATM-related kinase (ATR) inhibitor and cisplatin.Oncotarget · 2016Article
- ATR Kinase Inhibition Protects Non-cycling Cells from the Lethal Effects of DNA Damage and Transcription Stress.The Journal of biological chemistry · 2016Article
- Chk1 phosphorylated at serine345 is a predictor of early local recurrence and radio-resistance in breast cancer.Molecular oncology · 2016Article
- Molecular Pathways: Targeting ATR in Cancer Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Review
- VE-821, an ATR inhibitor, causes radiosensitization in human tumor cells irradiated with high LET radiation.Radiation oncology (London, England) · 2015Article
- Targeting the Checkpoint to Kill Cancer Cells.Biomolecules · 2015Review
- Pharmacologic inhibition of ATR and ATM offers clinically important distinctions to enhancing platinum or radiation response in ovarian, endometrial, and cervical cancer cells.Gynecologic oncology · 2015Article
- Critical role of lysine 134 methylation on histone H2AX for γ-H2AX production and DNA repair.Nature communications · 2014Article
- Radiosensitization of human leukemic HL-60 cells by ATR kinase inhibitor (VE-821): phosphoproteomic analysis.International journal of molecular sciences · 2014Article
- Src family kinases promote silencing of ATR-Chk1 signaling in termination of DNA damage checkpoint.The Journal of biological chemistry · 2014Article
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9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We compared the effects of inhibitors of kinases ATM (KU55933) and ATR (VE-821) (incubated for 30 min before irradiation) on the radiosensitization of human promyelocyte leukaemia cells (HL-60), lacking functional protein p53. VE-821 reduces phosphorylation of check-point kinase 1 at serine 345, and KU55933 reduces phosphorylation of check-point kinase 2 on threonine 68 as assayed 4 h after irradiation by the dose of 6 Gy. Within 24 h after gamma-irradiation with a dose of 3 Gy, the cells accumulated in the G2 phase (67 %) and the number of cells in S phase decreased. KU55933 (10 μM) did not affect the accumulation of cells in G2 phase and did not affect the decrease in the number of cells in S phase after irradiation. VE-821 (2 and 10 μM) reduced the number of irradiated cells in the G2 phase to the level of non-irradiated cells and increased the number of irradiated cells in S phase, compared to irradiated cells not treated with inhibitors. In the 144 h interval after irradiation with 3 Gy, there was a considerable induction of apoptosis in the VE-821 group (10 μM). The repair of the radiation damage, as observed 72 h after irradiation, was more rapid in the group exposed solely to irradiation and in the group treated with KU55933 (80 and 77 % of cells, respectively, were free of DSBs), whereas in the group incubated with 10 μM VE-821, there were only 61 % of cells free of DSBs. The inhibition of kinase ATR with its specific inhibitor VE-821 resulted in a more pronounced radiosensitizing effect in HL-60 cells as compared to the inhibition of kinase ATM with the inhibitor KU55933. In contrast to KU55933, the VE-821 treatment prevented HL-60 cells from undergoing G2 cell cycle arrest. Taken together, we conclude that the ATR kinase inhibition offers a new possibility of radiosensitization of tumour cells lacking functional protein p53.
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