ArticleMolecular cancer research : MCR2011
Methyl-binding domain protein 2-dependent proliferation and survival of breast cancer cells.
Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Gene regulatory mechanisms downstream of DNA methylation.Nature reviews. Genetics · 2026Review
- A potent small-chemical MBD2 inhibitor, KCC-07, induces selective cytotoxicity in hepatocellular and prostate cancer cells.Molecular biology reports · 2026Article
- Heterochromatome wide analyses reveal MBD2 as a phase separation scaffold for heterochromatin compartmentalization and composition.Nucleic acids research · 2025Article
- Loss of MBD2 is associated with tumor growth in small intestinal neuroendocrine tumors.Endocrine connections · 2025Article
- Mitochondria-localized MBD2c facilitates mtDNA transcription and drug resistance.Nature chemical biology · 2025Article
- Methyl-CpG binding domain protein 2 (Mbd2) drives breast cancer progression through the modulation of epithelial-to-mesenchymal transition.Experimental & molecular medicine · 2024Article
- Analysis of the complex between MBD2 and the histone deacetylase core of NuRD reveals key interactions critical for gene silencing.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- MBD2a-NuRD binds to the methylated γ-globin gene promoter and uniquely forms a complex required for silencing of HbF expression.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- MBD2 facilitates tumor metastasis by mitigating DDB2 expression.Cell death & disease · 2023Article
- Targeting TACC3 represents a novel vulnerability in highly aggressive breast cancers with centrosome amplification.Cell death and differentiation · 2023Article
- Hsa-miR-221-3p promotes proliferation and migration in HER2-positive breast cancer cells by targeting LASS2 and MBD2.Histology and histopathology · 2022Article
- Computational discovery of novel inhibitory candidates targeting versatile transcriptional repressor MBD2.Journal of molecular modeling · 2022Article
- Loss of MBD2 attenuates MLL-AF9-driven leukemogenesis by suppressing the leukemic cell cycle via CDKN1C.Oncogenesis · 2021Article
- Differential profiles of HDAC1 substrates and associated proteins in breast cancer cells revealed by trapping.Molecular omics · 2021Article
- Expression and clinical significance of methyl-CpG binding domain protein 2 in high-grade serous ovarian cancer.Oncology letters · 2020Article
- Demethylation of the NRF2 Promoter Protects Against Carcinogenesis Induced by Nano-SiOFrontiers in genetics · 2020Article
- Rational discovery of antimetastatic agents targeting the intrinsically disordered region of MBD2.Science advances · 2019Article
- The landscape of early carcinogenesis revealed through the lens of integrative genomics, epigenomics, and transcriptomics.Journal of thoracic disease · 2019Article
- Epigenetic biomarker screening by FLIM-FRET for combination therapy in ER+ breast cancer.Clinical epigenetics · 2019Article
- DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Methyl cytosine binding domain protein 2 (MBD2) has been shown to bind to and mediate repression of methylated tumor suppressor genes in cancer cells, where repatterning of CpG methylation and associated gene silencing is common. We have investigated the role of MBD2 in breast cancer cell growth and tumor suppressor gene expression. We show that stable short hairpin RNA (shRNA)-mediated knockdown of MBD2 leads to growth suppression of cultured human mammary epithelial cancer lines, SK-BR-3, MDA-MB-231, and MDA-MB-435. The peak antiproliferative occurs only after sustained, stable MBD2 knockdown. Once established, the growth inhibition persists over time and leads to a markedly decreased propensity for aggressive breast cancer cell lines to form in vivo xenograft tumors in Bagg Albino (BALB)/C nu/nu mice. The growth effects of MBD2 knockdown are accompanied by derepression of tumor suppressor genes, including DAPK1 and KLK10. Chromatin immunoprecipitation assays and bisulfite sequencing show MBD2 binding directly to the hyper methylated and CpG-rich promoters of both DAPK1 and KLK10. Remarkably, the promoter CpG island-associated methylation of these genes remained stable despite robust transcriptional activation in MBD2 knockdown cells. Expression of a shRNA-resistant MBD2 protein resulted in restoration of growth and resilencing of the MBD2-dependent tumor suppressor genes. Our data suggest that uncoupling CpG methylation from repressive chromatin remodeling and histone modifications by removing MBD2 is sufficient to initiate and maintain tumor suppressor gene transcription and suppress neoplastic cell growth. These results show a role for MBD2 in cancer progression and provide support for the prospect of targeting MBD2 therapeutically in aggressive breast cancers.
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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.