ArticleCancer biology & therapy2018
Deletion of MBD2 inhibits proliferation of chronic myeloid leukaemia blast phase cells.
Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- A potent small-chemical MBD2 inhibitor, KCC-07, induces selective cytotoxicity in hepatocellular and prostate cancer cells.Molecular biology reports · 2026Article
- The methyl-CpG binding domain 2 regulates peptidylarginine deiminase 4 expression and promotes neutrophil extracellular trap formation via the Janus kinase 2 signaling pathway in experimental severe asthma.Annals of medicine · 2025Article
- Versatile functions of methyl-CpG-binding domain 2 (MBD2) in cellular characteristics and differentiation.Molecular biology reports · 2025Review
- Novel insights into vancomycin-loaded calcium sulfate and negative pressure wound therapy in preventing infections in open fractures.Journal of orthopaedic surgery and research · 2024Article
- Methyl-CpG binding domain protein 2 (Mbd2) drives breast cancer progression through the modulation of epithelial-to-mesenchymal transition.Experimental & molecular medicine · 2024Article
- Effect of 5-Aza-2'-deoxycytidine on T-cell acute lymphoblastic leukemia cell biological behaviors and PTEN expression.CytoJournal · 2024Article
- Genetic or siRNA inhibition of MBD2 attenuates the UUO- and I/R-induced renal fibrosis via downregulation of EGR1.Molecular therapy. Nucleic acids · 2022Article
- Increased Methyl-CpG-Binding Domain Protein 2 Promotes Cigarette Smoke-Induced Pulmonary Hypertension.Frontiers in oncology · 2022Article
- Loss of MBD2 attenuates MLL-AF9-driven leukemogenesis by suppressing the leukemic cell cycle via CDKN1C.Oncogenesis · 2021Article
- LncRNAs and Rheumatoid Arthritis: From Identifying Mechanisms to Clinical Investigation.Frontiers in immunology · 2021Review
- Utilization of CRISPR-Mediated Tools for Studying Functional Genomics in Hematological Malignancies: An Overview on the Current Perspectives, Challenges, and Clinical Implications.Frontiers in genetics · 2021Review
- Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy.Frontiers in pharmacology · 2021Article
- Expression and clinical significance of methyl-CpG binding domain protein 2 in high-grade serous ovarian cancer.Oncology letters · 2020Article
- MBD2 Correlates with a Poor Prognosis and Tumor Progression in Renal Cell Carcinoma.OncoTargets and therapy · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant methylation of tumour suppressor genes is associated with the progression to a blast crisis in chronic myeloid leukaemia (CML). Methyl-CpG-binding domain protein 2 (MBD2) has been studied as a "reader" of DNA methylation in many cancers, but its role in CML is unclear. We constructed cell models of a homozygous deletion mutation of MBD2 using gene-editing technology in K562 cells and BV173 cells. Here, we demonstrated that the deletion of MBD2 inhibited cell proliferation capacity in vitro. MBD2 deletion also significantly inhibited K562 cell proliferation in a xenograft tumour model in vivo. Additionally, the JAK2/STAT3 signalling pathway, which is abnormally active in CML, was inhibited by MBD2 deletion, and MBD2 deletion could up-regulate the expression of SHP1. In conclusion, our findings suggest that MBD2 is a candidate therapeutic strategy for the CML blast phase.
Indexed as
Identifiers
What OpenQuestion holds
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.