ArticleInternational journal of cancer2012
DNA methylation-mediated silencing of nonsteroidal anti-inflammatory drug-activated gene (NAG-1/GDF15) in glioma cell lines.
Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- 6-Gingerol enhances the anti-tumor activity of temozolomide by inhibiting EGR1/GDF15 signaling in glioblastoma.Scientific reports · 2025Article
- The dark side of the light (UVA): melanoma microenvironment and cell survival strategies.Cell death discovery · 2025Article
- Curcumin-Induced Molecular Mechanisms in U-87 MG Glioblastoma Cells: Insights from Global Gene Expression Profiling.Molecules (Basel, Switzerland) · 2025Article
- Exposure to a Titanium Dioxide Product Alters DNA Methylation in Human Cells.Nanomaterials (Basel, Switzerland) · 2024Article
- GDF15/MIC-1: a stress-induced immunosuppressive factor which promotes the aging process.Biogerontology · 2024Review
- Interleukin 4 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- Batokine in Central Nervous System Diseases.Molecular neurobiology · 2023Review
- Overexpression of NAG-1/GDF15 prevents hepatic steatosis through inhibiting oxidative stress-mediated dsDNA release and AIM2 inflammasome activation.Redox biology · 2022Article
- Article
- NSAIDs and Cancer Resolution: New Paradigms beyond Cyclooxygenase.International journal of molecular sciences · 2022Review
- Emerging roles of growth differentiation factor-15 in brain disorders (Review).Experimental and therapeutic medicine · 2021Review
- Transcriptional Regulation of GDF15 by EGR1 Promotes Head and Neck Cancer Progression through a Positive Feedback Loop.International journal of molecular sciences · 2021Article
- Post-translational modification of Parkin and its research progress in cancer.Cancer communications (London, England) · 2019Review
- Coordinated Expression of Ras Suppressor 1 (RSU-1) and Growth Differentiation Factor 15 (GDF15) Affects Glioma Cell Invasion.Cancers · 2019Article
- Growth differentiation factor 15 (GDF15): A survival protein with therapeutic potential in metabolic diseases.Pharmacology & therapeutics · 2019Review
- Mechanism of methylation and acetylation of highHeliyon · 2019Review
- EZH2-Mediated Epigenetic Suppression of GDF15 Predicts a Poor Prognosis and Regulates Cell Proliferation in Non-Small-Cell Lung Cancer.Molecular therapy. Nucleic acids · 2018Article
- Distinct response to GDF15 knockdown in pediatric and adult glioblastoma cell lines.Journal of neuro-oncology · 2018Article
- Review
- Potential Epigenetic-Based Therapeutic Targets for Glioma.Frontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Nonsteroidal anti-inflammatory drug-activated gene, NAG-1, a transforming growth factor-β member, is involved in tumor progression and development. The association between NAG-1 expression and development and progression of glioma has not been well defined. Glioblastoma cell lines have lower basal expression of NAG-1 than other gliomas and normal astrocytes. Most primary human gliomas have very low levels of NAG-1 expression. NAG-1 basal expression appeared to inversely correlate with tumor grade in glioma. Aberrant promoter hypermethylation is a common mechanism for silencing of tumor suppressor genes in cancer cells. In glioblastoma cell lines, NAG-1 expression was increased by the demethylating agent, 5-aza-2'-deoxycytidine. To investigate whether the NAG-1 gene was silenced by hypermethylation in glioblastoma, we examined DNA methylation status using genomic bisulfite sequencing. The NAG-1 promoter was densely methylated in several glioblastoma cell lines as well as in primary oligodendroglioma tumor samples, which have low basal expression of NAG-1. DNA methylation at two specific sites (-53 and +55 CpG sites) in the NAG-1 promoter was strongly associated with low NAG-1 expression. The methylation of the NAG-1 promoter at the -53 site blocks Egr-1 binding and thereby suppresses Nag-1 induction. Treatment of cells with low basal NAG-1 expression with NAG-1 inducer also did not increase NAG-1. Incubation with a demethylation chemical increased Nag-1 basal expression and subsequent incubation with a NAG-1 inducer increased NAG-1 expression. We concluded from these data that methylation of specific promoter sequences causes transcriptional silencing of the NAG-1 locus in glioma and may ultimately contribute to tumor progression.
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