ArticleCancer research2011
Overexpression of MBD2 in glioblastoma maintains epigenetic silencing and inhibits the antiangiogenic function of the tumor suppressor gene BAI1.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 80 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- The PKA/MBD2 Axis Transcriptionally Represses INPP5A to Modulate PI3K/Akt Signaling and Accelerate Pituitary Tumorigenesis.CNS neuroscience & therapeutics · 2026Article
- Functional diversity of BAI1 (ADGRB1): From angiostasis to synaptic remodeling and disease therapeutics.iScience · 2026Review
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- Loss of MBD2 is associated with tumor growth in small intestinal neuroendocrine tumors.Endocrine connections · 2025Article
- KCC-07, MBD2 Inhibitor, Expands the Therapeutic Window of DNA Damage Inducing Reagents in Neural Tumor Cells.Experimental neurobiology · 2025Article
- Targeting redox-sensitive MBD2-NuRD condensate in cancer cells.Nature cell biology · 2025Article
- Recent advances in research on common targets of neurological and sex hormonal influences on asthma.Clinical and translational allergy · 2025Review
- Novel Isoforms of Adhesion G Protein-Coupled Receptor B1 (ADGRB1/BAI1) Generated from an Alternative Promoter in Intron 17.Molecular neurobiology · 2025Article
- Transcriptional landscape of the interaction of human Mesenchymal Stem Cells with Glioblastoma in bioprinted co-cultures.Stem cell research & therapy · 2024Article
- CircUGP2 Suppresses Intrahepatic Cholangiocarcinoma Progression via p53 Signaling Through Interacting With PURB to Regulate ADGRB1 Transcription and Sponging miR-3191-5p.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Epigenetic reprogramming shapes the cellular landscape of schwannoma.Nature communications · 2024Article
- The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development.International journal of molecular sciences · 2023Review
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- Construction of a Prognostic Model Based on Methylation-Related Genes in Patients with Colon Adenocarcinoma.Cancer management and research · 2023Article
- Targeted Epigenetic Interventions in Cancer with an Emphasis on Pediatric Malignancies.Biomolecules · 2022Review
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Computational discovery of novel inhibitory candidates targeting versatile transcriptional repressor MBD2.Journal of molecular modeling · 2022Article
- Sox9 directs divergent epigenomic states in brain tumor subtypes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Beyond the marks: reader-effectors as drivers of epigenetics and chromatin engineering.Trends in biochemical sciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Brain angiogenesis inhibitor 1 (BAI1) is a putative G protein-coupled receptor with potent antiangiogenic and antitumorigenic properties that is mutated in certain cancers. BAI1 is expressed in normal human brain, but it is frequently silenced in glioblastoma multiforme. In this study, we show that this silencing event is regulated by overexpression of methyl-CpG-binding domain protein 2 (MBD2), a key mediator of epigenetic gene regulation, which binds to the hypermethylated BAI1 gene promoter. In glioma cells, treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-Aza-dC) was sufficient to reactivate BAI1 expression. Chromatin immunoprecipitation showed that MBD2 was enriched at the promoter of silenced BAI1 in glioma cells and that MBD2 binding was released by 5-Aza-dC treatment. RNA interference-mediated knockdown of MBD2 expression led to reactivation of BAI1 gene expression and restoration of BAI1 functional activity, as indicated by increased antiangiogenic activity in vitro and in vivo. Taken together, our results suggest that MBD2 overexpression during gliomagenesis may drive tumor growth by suppressing the antiangiogenic activity of a key tumor suppressor. These findings have therapeutic implications because inhibiting MBD2 could offer a strategy to reactivate BAI1 and suppress glioma pathobiology.
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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.