ArticleScientific reports2015
DNA methyltransferase 3A promotes cell proliferation by silencing CDK inhibitor p18INK4C in gastric carcinogenesis.
Article in Scientific reports, 2015. 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, 25 citations in OpenAlex.
- Exposure to electronic cigarette aerosols triggers alterations in genomic DNA methylation that impacts cancer pathways in mice.Inhalation toxicology · 2026Article
- CIP/KIP and INK4 families as hostages of oncogenic signaling.Cell division · 2024Review
- Clinical significance of cyclin-dependent kinase inhibitor 2C expression in cancers: from small cell lung carcinoma to pan-cancers.BMC pulmonary medicine · 2022Article
- LINC00673 Represses CDKN2C and Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells by EZH2-Mediated H3K27 Trimethylation.Frontiers in oncology · 2020Article
- Brief review: Can modulating DNA methylation state help the clinical application of oligodendrocyte precursor cells as a source of stem cell therapy?Brain research · 2019Review
- Role of DNA Methylation in the Development and Differentiation of Intestinal Epithelial Cells and Smooth Muscle Cells.Journal of neurogastroenterology and motility · 2019Review
- Article
- APC gene is modulated by hsa-miR-135b-5p in both diffuse and intestinal gastric cancer subtypes.BMC cancer · 2018Article
- Article
- Epigenetic Mistakes in Neurodevelopmental Disorders.Journal of molecular neuroscience : MN · 2017Review
- Repression of CDKN2C caused by PML/RARα binding promotes the proliferation and differentiation block in acute promyelocytic leukemia.Frontiers of medicine · 2016Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known about the roles of DNA methyltransferase 3A (DNMT3A) in gastric carcinogenesis. Here, we reported that the exogenous expression of DNMT3A promoted gastric cancer (GC) cell proliferation by accelerating the G1/S transition. Subsequently, p18INK4C was identified as a downstream target of DNMT3A. The elevated expression of DNMT3A suppressed p18INK4C at least at the transcriptional level. Depletion of p18INK4C expression in GC cells induced cell cycle progression, whereas its re-expression alleviated the effect of DNMT3A overexpression on G1/S transition. Furthermore, we found that DNMT3A modulated p18INK4C by directly binding to and silencing the p18INK4C gene via promoter hypermethylation. In clinical GC tissue specimens analyzed, the level of methylation of p18INK4C detected in tumor tissues was significantly higher than that in paired non-tumor tissues. Moreover, elevated level of DNMT3A expression was associated with the differentiation of GC tissues and was negatively correlated with the p18INK4C expression level. Taken together, our results found that DNMT3A contributes to the dysregulation of the cell cycle by repressing p18INK4C in a DNA methylation-dependent manner, suggesting that DNMT3A-p18INK4C axis involved in GC. These findings provide new insights into gastric carcinogenesis and a potential therapeutic target for GC that may be further investigated in the future.
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