ArticlePloS one2015
A New Epigenetic Mechanism of Temozolomide Action in Glioma Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 99 citations in OpenAlex.
- Dexamethasone Modulates Global DNA Methylation and Oxidative DNA Damage in Glioblastoma Cell Lines.Cells · 2026Article
- Targeting Ferroptosis in Glioblastoma: Molecular Mechanisms, Tumor Microenvironment, and Therapeutic Opportunities.Cancers · 2026Review
- Therapeutic Potential of Tetrandrine Compared to Temozolomide in Treating Glioblastoma Multiforme Under Normoxic and Hypoxic Conditions.International journal of molecular sciences · 2026Article
- Phytocannabinoids as epigenetic regulators: bridging DNA methylation and redox homeostasis in glioblastoma.Journal of applied genetics · 2026Article
- Association Between MGMT Promoter Methylation and Clinical and Lifestyle Factors in Glioblastoma: A Single-Center Study in Korea.Journal of clinical medicine · 2026Article
- AquIRE reveals the mechanisms of clinically induced RNA damage and the conservation and dynamics of glycoRNAs.Nucleic acids research · 2026Article
- Article
- The epigenetic mechanisms involved in the treatment resistance of glioblastoma.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Article
- Epigenetic Characteristics in Primary and Recurrent Glioblastoma-Influence on the Clinical Course.Biomedicines · 2024Article
- Mechanistic Insights on Metformin and Arginine Implementation as Repurposed Drugs in Glioblastoma Treatment.International journal of molecular sciences · 2024Article
- Minimally-invasive implantable device enhances brain cancer suppression.EMBO molecular medicine · 2024Article
- Emerging Therapies for Glioblastoma.Cancers · 2024Review
- Naringin and temozolomide combination suppressed the growth of glioblastoma cells by promoting cell apoptosis: network pharmacology,Frontiers in pharmacology · 2024Article
- A receptor-mediated landscape of druggable and targeted nanomaterials for gliomas.Materials today. Bio · 2023Review
- BLM helicase overexpressed in human gliomas contributes to diverse responses of human glioma cells to chemotherapy.Cell death discovery · 2023Article
- Juglone in Combination with Temozolomide Shows a Promising Epigenetic Therapeutic Effect on the Glioblastoma Cell Line.International journal of molecular sciences · 2023Article
- Drug Permeability: From the Blood-Brain Barrier to the Peripheral Nerve Barriers.Advanced therapeutics · 2023Article
- Influence of MMR, MGMT Promotor Methylation and Protein Expression on Overall and Progression-Free Survival in Primary Glioblastoma Patients Treated with Temozolomide.International journal of molecular sciences · 2023Article
- Glioblastoma-Derived Small Extracellular Vesicles: Nanoparticles for Glioma Treatment.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temozolomide (TMZ) is an oral alkylating chemotherapeutic agent that prolongs the survival of patients with glioblastoma (GBM). Despite that high TMZ potential, progression of disease and recurrence are still observed. Therefore a better understanding of the mechanism of action of this drug is necessary and may allow more durable benefit from its anti-glioma properties. Using nucleotide post-labelling method and separation on thin-layer chromatography we measured of global changes of 5-methylcytosine (m5C) in DNA of glioma cells treated with TMZ. Although m5C is not a product of TMZ methylation reaction of DNA, we analysed the effects of the drug action on different glioma cell lines through global changes at the level of the DNA main epigenetic mark. The first effect of TMZ action we observed is DNA hypermethylation followed by global demethylation. Therefore an increase of DNA methylation and down regulation of some genes expression can be ascribed to activation of DNA methyltransferases (DNMTs). On the other hand hypomethylation is induced by oxidative stress and causes uncontrolled expression of pathologic protein genes. The results of brain tumours treatment with TMZ suggest the new mechanism of modulation epigenetic marker in cancer cells. A high TMZ concentration induced a significant increase of m5C content in DNA in the short time, but a low TMZ concentration at longer time hypomethylation is observed for whole range of TMZ concentrations. Therefore TMZ administration with low doses of the drug and short time should be considered as optimal therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.