ArticleBMC medical genetics2013
The promoter of miR-663 is hypermethylated in Chinese pediatric acute myeloid leukemia (AML).
Article in BMC medical genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- miR-370 is better than miR-375 as a non-invasive diagnostic biomarker for pediatric acute myeloid leukemia patients.Cancer biomarkers : section A of Disease markers · 2022Article
- Analysis of promoter methylation and epigenetic regulation of miR-32 in colorectal cancer cells.Experimental and therapeutic medicine · 2019Article
- MiRNA Dysregulation in Childhood Hematological Cancer.International journal of molecular sciences · 2018Review
- Review
- Use of methylation profiling to identify significant differentially methylated genes in bone marrow mesenchymal stromal cells from acute myeloid leukemia.International journal of molecular medicine · 2018Article
- Epigenetic modification of miR-663 controls mitochondria-to-nucleus retrograde signaling and tumor progression.The Journal of biological chemistry · 2017Article
- Genome-wide DNA methylation sequencing reveals miR-663a is a novel epimutation candidate in CIMP-high endometrial cancer.International journal of oncology · 2017Article
- MicroRNA promoter methylation: a new tool for accurate detection of urothelial carcinoma.British journal of cancer · 2017Article
- MicroRNAs and regulated interaction networks reveal differences between adult and pediatric acute myeloid leukemia.International journal of clinical and experimental pathology · 2017Article
- Therapeutic Resistance in Acute Myeloid Leukemia: The Role of Non-Coding RNAs.International journal of molecular sciences · 2016Review
- Diagnostic & prognostic role of microRNAs in paediatric acute myeloid leukaemia.The Indian journal of medical research · 2016Review
- ZNF224, Krüppel like zinc finger protein, induces cell growth and apoptosis-resistance by down-regulation of p21 and p53 via miR-663a.Oncotarget · 2016Article
- MicroRNA-663a is downregulated in non-small cell lung cancer and inhibits proliferation and invasion by targeting JunD.BMC cancer · 2016Article
- Article
- Analysis of a four generation family reveals the widespread sequence-dependent maintenance of allelic DNA methylation in somatic and germ cells.Scientific reports · 2016Article
- Article
- Hypermethylation of the GATA binding protein 4 (GATA4) promoter in Chinese pediatric acute myeloid leukemia.BMC cancer · 2015Article
- Global characteristics of childhood acute promyelocytic leukemia.Blood reviews · 2015Review
- APP intracellular domain acts as a transcriptional regulator of miR-663 suppressing neuronal differentiation.Cell death & disease · 2015Article
- Early B-cell factor 3 (EBF3) is a novel tumor suppressor gene with promoter hypermethylation in pediatric acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2015Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is growing evidence supporting a role for microRNAs (miRNA) as targets in aberrant mechanisms of DNA hypermethylation. Epigenetic silencing of tumor suppressor miRNAs, including miR-663, which has recently been reported to be inactivated by hypermethylation in several cancers, may play important roles in pediatric acute myeloid leukemia (AML). However, expression of miR-663 and its promoter methylation remain status unclear in childhood leukemia.
methodsPromoter methylation status of miR-663 was investigated by methylation specific PCR (MSP) and bisulfate genomic sequencing (BGS). Transcriptional expression of miR-663 was evaluated by semi-quantitative and real-time PCR, and the relationship between expression of miR-663 and promoter methylation was confirmed using 5-aza-2'-deoxycytidine (5-Aza) demethylation reagent.
resultsMiR-663 was aberrantly methylated in 45.5% (5/11) leukemia cell lines; BGS showed that the promoter was significantly methylated in three AML cell lines; methylation of miR-663 was significantly higher in Chinese pediatric AML patients [41.4% (29/70)] compared to normal bone marrow (NBM) control samples [10.0% (3/30)]. These results were confirmed by both BGS and 5-Aza demethylation analysis. In addition, miR-663 transcript expression was significantly lower in AML patients, both with and without miR-663 methylation, compared to controls; however, there were no significant differences in clinical features or French-American-British (FAB) classification between patients with and without miR-663 methylation.
conclusionsExpression of miR-663 was significantly lower in pediatric AML cells compared to NBM controls; furthermore, a high frequency of miR-663 promoter hypermethylation was observed in both AML cell lines and pediatric AML samples. Inactivation of miR-663 by promoter hypermethylation could be affected by 5-Aza demethylation. These findings suggest that hypermethylation of the miR-663 promoter may be an early event in the development of pediatric AML.
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