ArticleEpigenetics2016
Epigenetic silencing of AKAP12 in juvenile myelomonocytic leukemia.
Article in Epigenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Metastasis suppressor genes in clinical practice: are they druggable?Cancer metastasis reviews · 2023Review
- Potential of blood-based biomarker approaches in endometrium and breast cancer: a case-control comparison study.Archives of gynecology and obstetrics · 2022Article
- Identification of cystic fibrosis transmembrane conductance regulator as a prognostic marker for juvenile myelomonocytic leukemia via the whole-genome bisulfite sequencing of monozygotic twins and data mining.Translational pediatrics · 2022Article
- Review
- Current Treatment of Juvenile Myelomonocytic Leukemia.Journal of clinical medicine · 2021Review
- International Consensus Definition of DNA Methylation Subgroups in Juvenile Myelomonocytic Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Development and Validation of a Prognostic Nomogram Based on DNA Methylation-Driven Genes for Patients With Ovarian Cancer.Frontiers in genetics · 2021Article
- Single-Center Experience With Epigenetic Treatment for Juvenile Myelomonocytic Leukemia.Frontiers in oncology · 2020Article
- Gene mutations do not operate in a vacuum: the increasing importance of epigenetics in juvenile myelomonocytic leukemia.Epigenetics · 2019Review
- ASB1 differential methylation in ischaemic cardiomyopathy: relationship with left ventricular performance in end-stage heart failure patients.ESC heart failure · 2018Article
- Curcumol Controls Choriocarcinoma Stem-Like Cells Self-Renewal via Repression of DNA Methyltransferase (DNMT)- and Histone Deacetylase (HDAC)-Mediated Epigenetic Regulation.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- RAS-pathway mutation patterns define epigenetic subclasses in juvenile myelomonocytic leukemia.Nature communications · 2017Article
- Epigenetic dysregulation of the erythropoietic transcription factor KLF1 and the β-like globin locus in juvenile myelomonocytic leukemia.Epigenetics · 2017Article
- Turning the tide in myelodysplastic/myeloproliferative neoplasms.Nature reviews. Cancer · 2017Review
- CREBBP is a target of epigenetic, but not genetic, modification in juvenile myelomonocytic leukemia.Clinical epigenetics · 2016Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A-kinase anchor protein 12 (AKAP12) is a regulator of protein kinase A and protein kinase C signaling, acting downstream of RAS. Epigenetic silencing of AKAP12 has been demonstrated in different cancer entities and this has been linked to the process of tumorigenesis. Here, we used quantitative high-resolution DNA methylation measurement by MassARRAY to investigate epigenetic regulation of all three AKAP12 promoters (i.e., α, β, and γ) within a large cohort of juvenile myelomonocytic leukemia (JMML) patient samples. The AKAP12α promoter shows DNA hypermethylation in JMML samples, which is associated with decreased AKAP12α expression. Promoter methylation of AKAP12α correlates with older age at diagnosis, elevated levels of fetal hemoglobin and poor prognosis. In silico screening for transcription factor binding motifs around the sites of most pronounced methylation changes in the AKAP12α promoter revealed highly significant scores for GATA-2/-1 sequence motifs. Both transcription factors are known to be involved in the haematopoietic differentiation process. Methylation of a reporter construct containing this region resulted in strong suppression of AKAP12 promoter activity, suggesting that DNA methylation might be involved in the aberrant silencing of the AKAP12 promoter in JMML. Exposure to DNMT- and HDAC-inhibitors reactivates AKAP12α expression in vitro, which could potentially be a mechanism underlying clinical treatment responses upon demethylating therapy. Together, these data provide evidence for epigenetic silencing of AKAP12α in JMML and further emphasize the importance of dysregulated RAS signaling in JMML pathogenesis.
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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.