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Quercetin exhibits cytotoxicity in cancer cells by inducing two-ended DNA double-strand breaks.
Biochem Biophys Res Commun
December 2024
Graduate School of Science and Technology, Gunma University, Kiryu, 376-8515, Japan; Graduate School of Nanobioscience, Yokohama City University, Yokohama, 236-0027, Japan; Gunma University Center for Food and Science and Wellness, Gunma University, Kiryu, 376-8515, Japan. Electronic address:
Article Synopsis
- Quercetin, a flavonoid with antioxidant properties, can induce DNA double-strand breaks (DSBs) in a concentration-dependent manner, but the exact mechanism behind this effect is still unclear.
- The study used HeLa cells and gene-knockout cell lines to investigate that quercetin does not primarily involve DNA topoisomerase II (Top2) in inducing DSBs; instead, a transient accumulation of reactive oxygen species (ROS) is linked to this process.
- The DSBs caused by quercetin are mainly repaired through non-homologous end-joining and homologous recombination, suggesting it could be used as a radiomimetic agent with effects similar to X-ray exposure.
TORC2 inhibition triggers yeast chromosome fragmentation through misregulated Base Excision Repair of clustered oxidation events.
Nat Commun
November 2024
Friedrich Miescher Institute for Biomedical Research, Fabrikstrasse 24, Basel, Switzerland.
Combinational therapies provoking cell death are of major interest in oncology. Combining TORC2 kinase inhibition with the radiomimetic drug Zeocin results in a rapid accumulation of double-strand breaks (DSB) in the budding yeast genome. This lethal Yeast Chromosome Shattering (YCS) requires conserved enzymes of base excision repair.
View Article and Find Full Text PDFSMAD4 Limits PARP1 dependent DNA Repair to Render Pancreatic Cancer Cells Sensitive to Radiotherapy.
Cell Death Dis
November 2024
Department of Gastroenterology, Huadong Hospital, Fudan University, 200040, Shanghai, China.
Dysregulation of SMAD4 (i.e. somatic mutation) is strongly associated with poor pancreatic ductal adenocarcinoma (PDAC) prognosis, yet the molecular mechanisms remain underlying this relationship obscure.
View Article and Find Full Text PDFThrombopoietin mimetic reduces mouse lung inflammation and fibrosis after radiation by attenuating activated endothelial phenotypes.
JCI Insight
November 2024
Department of Radiation Oncology.
Radiation-induced lung injury (RILI) initiates radiation pneumonitis and progresses to fibrosis as the main side effect experienced by patients with lung cancer treated with radiotherapy. There is no effective drug for RILI. Sustained vascular activation is a major contributor to the establishment of chronic disease.
View Article and Find Full Text PDFImpact of Optimized Ku-DNA Binding Inhibitors on the Cellular and In Vivo DNA Damage Response.
Cancers (Basel)
September 2024
Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Article Synopsis
- DNA-dependent protein kinase (DNA-PK) plays a crucial role in repairing DNA double-strand breaks and is a target for cancer therapies to enhance the effectiveness of radiation treatments.
- Researchers have developed new oxindole Ku-DNA binding inhibitors (Ku-DBis) that show better cellular uptake and strong inhibition of Ku proteins, demonstrating variable effectiveness across different non-small cell lung cancer (NSCLC) cell lines.
- In vivo studies reveal that Ku-DBis can block DNA-PK autophosphorylation, alter DNA damage responses, and lower tumor cell growth, indicating their potential use in improving cancer treatment outcomes.
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