ArticleThe Journal of clinical endocrinology and metabolism2022
Aspirin Mediates Its Antitumoral Effect Through Inhibiting PTTG1 in Pituitary Adenoma.
Article in The Journal of clinical endocrinology and metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- The role of methylation in pituitary neuroendocrine tumors current insights and emerging perspectives.Molecular biology reports · 2026Review
- Defactinib in Combination with Mitotane Can Be an Effective Treatment in Human Adrenocortical Carcinoma.International journal of molecular sciences · 2025Article
- DNA Methylation in Pituitary Adenomas: A Scoping Review.International journal of molecular sciences · 2025Article
- Research progress on nonsteroidal anti-inflammatory drugs in the treatment of pituitary neuroendocrine tumors.Frontiers in pharmacology · 2024Review
- Integrative Analysis of the Role ofCurrent issues in molecular biology · 2023Article
- PTTG1 Enhances Oncolytic Adenovirus 5 Entry into Pancreatic Adenocarcinoma Cells by Increasing CXADR Expression.Viruses · 2023Article
- Context-Dependent Role of Glucocorticoid Receptor Alpha and Beta in Breast Cancer Cell Behaviour.Cells · 2023Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
contextDNA demethylation and inhibitory effects of aspirin on pituitary cell proliferation have been demonstrated.
objectiveOur aim was to clarify the molecular mechanisms behind the aspirin-related effects in pituitary cells.
methodsDNA methylome and whole transcriptome profile were investigated in RC-4B/C and GH3 pituitary cell lines upon aspirin treatment. Effects of aspirin and a demethylation agent, decitabine, were further tested in vitro. PTTG1 expression in 41 human PitNET samples and whole genome gene and protein expression data of 76 PitNET and 34 control samples (available in Gene Expression Omnibus) were evaluated.
resultsAspirin induced global DNA demethylation and consequential transcriptome changes. Overexpression of Tet enzymes and their cofactor Uhrf2 were identified behind the increase of 5-hydroxymethylcytosine (5hmC). Besides cell cycle, proliferation, and migration effects that were validated by functional experiments, aspirin increased Tp53 activity through p53 acetylation and decreased E2f1 activity. Among the p53 controlled genes, Pttg1 and its interacting partners were downregulated upon aspirin treatment by inhibiting Pttg1 promoter activity. 5hmC positively correlated with Tet1-3 and Tp53 expression, and negatively correlated with Pttg1 expression, which was reinforced by the effect of decitabine. Additionally, high overlap (20.15%) was found between aspirin-regulated genes and dysregulated genes in PitNET tissue samples.
conclusionA novel regulatory network has been revealed, in which aspirin regulated global demethylation, Tp53 activity, and Pttg1 expression along with decreased cell proliferation and migration. 5hmC, a novel tissue biomarker in PitNET, indicated aspirin antitumoral effect in vitro as well. Our findings suggest the potential beneficial effect of aspirin in PitNET.
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