Objectives: The dental resin monomer triethylene glycol dimethacrylate (TEGDMA) caused a cell cycle arrest in response to DNA damage. However, the underlying mechanisms are unclear. Therefore, the influence of TEGDMA on the cell cycle was analyzed in comparison with the chemotherapeutic agents adriamycin and mitomycin C (MMC), which arrest the cell cycle through different mechanisms.
Methods: RAW264.7 mouse macrophages were exposed to TEGDMA, adriamycin, or MMC, and flow cytometry (FACS) was used for cell cycle analyses. In addition, the number of surviving cells was determined by a crystal violet assay, and viability in treated cultures was determined by FACS after staining of cells with trypan blue. Morphological changes in cells were interpreted using forward and side scatter (FSC/SSC) cell physical criteria.
Results: The exposure of cells to 1mM TEGDMA resulted in a delay of the cell cycle in G1 phase since 85.3% of the cells were found in G1 compared with 47.4% in untreated controls. Adriamycin also increased the number of cells (72.1%) in G1 compared to controls. Caffeine, an inhibitor of the checkpoint kinases ATM (ataxia telangiectasia-mutated) and ATR (ATM and Rad3-related), had no effect on the TEGDMA and adriamycin-induced cell cycle arrest. In contrast, MMC delayed the cell cycle in G2 since cell numbers increased to 22.1% compared to 10.7% in controls. The effect of MMC on G2 was even increased by low caffeine concentrations (100-400muM), but 1000muM caffeine inhibited MMC activity.
Significance: Our results suggest that the mechanism of a TEGDMA-induced arrest of the cell cycle is different from the effect of the direct-acting interstrand crosslinking agent MMC. Since TEGDMA produced oxidative stress, it probably acts indirectly on the cell cycle through reactive oxygen species, unless TEGDMA-DNA adducts are shown experimentally.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.dental.2009.10.005 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
PI3K/AKT/mTOR Targeting in Colorectal Cancer Radiotherapy: A Systematic Review.
J Gastrointest Cancer
January 2025
Medical Physics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Background: Radioresistance is a major challenge in the treatment of patients with colorectal cancer (CRC) and impairs the efficacy of radiotherapy. The PI3K/AKT/mTOR signaling pathway plays a critical role in CRC and contributes to the development of radioresistance. Accordingly, targeting this signaling pathway may be a promising strategy to improve oncotherapy.
View Article and Find Full Text PDFSalt-in-presalt electrolyte solutions for high-potential non-aqueous sodium metal batteries.
Nat Nanotechnol
January 2025
Department of Chemical and Biomolecular Engineering, University of Maryland, College Park, MD, USA.
Room-temperature non-aqueous sodium metal batteries are viable candidates for cost-effective and safe electrochemical energy storage. However, they show low specific energy and poor cycle life as the use of conventional organic-based non-aqueous electrolyte solutions enables the formation of interphases that cannot prevent degradations at the positive and negative electrodes. Here, to promote the formation of inorganic NaF-rich interphases on both negative and positive electrodes, we propose the salt-in-presalt (SIPS) electrolyte formulation strategy.
View Article and Find Full Text PDFThe kinetics of uracil-N-glycosylase distribution inside replication foci.
Sci Rep
January 2025
Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacký University Olomouc, Olomouc, Czech Republic.
Mismatched nucleobase uracil is commonly repaired through the base excision repair initiated by DNA uracil glycosylases. The data presented in this study strongly indicate that the nuclear uracil-N-glycosylase activity and nuclear protein content in human cell lines is highest in the S phase of the cell cycle and that its distribution kinetics partially reflect the DNA replication activity in replication foci. In this respect, the data demonstrate structural changes of the replication focus related to the uracil-N-glycosylase distribution several dozens of minutes before end of its replication.
View Article and Find Full Text PDFIdentification of potential biomarkers for 2022 Mpox virus infection: a transcriptomic network analysis and machine learning approach.
Sci Rep
January 2025
Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet, 3114, Bangladesh.
Monkeypox virus (MPXV), a zoonotic pathogen, re-emerged in 2022 with the Clade IIb variant, raising global health concerns due to its unprecedented spread in non-endemic regions. Recent studies have shown that Clade IIb (2022 MPXV) is marked by unique genomic mutations and epidemiological behaviors, suggesting variations in host-virus interactions. This study aimed to identify the differentially expressed genes (DEGs) induced by the 2022 MPXV infection through comprehensive bioinformatics analyses of microarray and RNA-Seq datasets from post-infected cell types with different MPXV clades.
View Article and Find Full Text PDFHigh-resolution analysis of human centromeric chromatin.
Life Sci Alliance
April 2025
National Cancer Institute, Center for Cancer Research, Laboratory of Receptor Biology and Gene Expression, Bethesda, MD, USA
Centromeres are marked by the centromere-specific histone H3 variant CENP-A/CENH3. Throughout the cell cycle, the constitutive centromere-associated network is bound to CENP-A chromatin, but how this protein network modifies CENP-A nucleosome conformations in vivo is unknown. Here, we purify endogenous centromeric chromatin associated with the CENP-C complex across the cell cycle and analyze the structures by single-molecule imaging and biochemical assays.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!