ArticleClinical epigenetics2019
Diuron exposure and Akt overexpression promote glioma formation through DNA hypomethylation.
Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Radiogenomic profiling of global DNA methylation associated with molecular phenotypes and immune features in glioma.BMC medicine · 2024Article
- Tracking Targets of Dynamic Super-EnhancersEnvironmental health perspectives · 2023Article
- Epigenetic modifications: Critical participants of the PD‑L1 regulatory mechanism in solid tumors (Review).International journal of oncology · 2022Review
- Article
- Palmitoyl transferases act as potential regulators of tumor-infiltrating immune cells and glioma progression.Molecular therapy. Nucleic acids · 2022Article
- The DCMU Herbicide Shapes T-cell Functions By Modulating Micro-RNA Expression Profiles.Frontiers in immunology · 2022Article
- Comprehensive Analysis of the Immune Cell Infiltration Landscape and Immune-Related Methylation in Retinoblastoma.Frontiers in genetics · 2022Article
- DNA Methylation-Driven Genes for Developing Survival Nomogram for Low-Grade Glioma.Frontiers in oncology · 2021Article
- Identification and Validation of Immune-Related Methylation Clusters for Predicting Immune Activity and Prognosis in Breast Cancer.Frontiers in immunology · 2021Article
- Low Expression of APOB mRNA or Its Hypermethylation Predicts Favorable Overall Survival in Patients with Low-Grade Glioma.OncoTargets and therapy · 2020Article
- Drug resistance in glioblastoma: are persisters the key to therapy?Cancer drug resistance (Alhambra, Calif.) · 2020Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiuron is an environmental component listed as a likely human carcinogen. Several other studies report that diuron can be oncogenic for bladder, urothelial, skin, and mammary cells. No study mentions the putative effect of diuron on the glioma occurrence.
objectivesWe here wanted to investigate the effects of diuron exposure on the glioma occurrence while wishing to incriminate a putative implication of DNA methylation modulation in this process.
methodsIn in vivo model of glioma, diuron exposure was firstly compared or combined with oncogenic overexpressions already known to promote gliomagenesis. ELISA quantifying the 5-methylcytosine level on DNA was performed to examine the global DNA methylation level. Quantitative real-time polymerase chain reaction and proximity ligation in situ assay were performed to identify the molecular causes of the diuron-induced changes of DNA methylation. The signatures diuron-induced changes of DNA methylation were analyzed in a cohort of 23 GBM patients.
resultsDiuron exposure is not sufficient to promote glioma, such as the oncogenic overexpression of Akt or Ras. However, the combination of diuron exposure and Akt overexpression promotes glioma. We observed that the diuron/Akt-induced glioma is characterized by three phenotypic signatures characterizing cancer cells: a global DNA hypomethylation, a loss of sensitivity to cell death induction, and a gain of signals of immune escape. Our data associated these phenotypes with three aberrant DNA methylation signatures: the LLT1, PD-L1, and Bcl-w hypomethylations. Strikingly, we observed that these three concomitant hypomethylations were only observed in GBM patients having a potential exposure to diuron via their professional activity.
conclusionsAs single player, diuron is not an oncogenic of glioma, but it can participate to the glioma formation in association with other events (also devoid of oncogenic property as single player) such as Akt overexpression.
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