Identification of imprinting regulators at the Meg3 differentially methylated region

McMurray, Erin N.; Schmidt, Jennifer V.

doi:10.1016/j.ygeno.2012.06.001

Cited by 24 publications

(19 citation statements)

References 50 publications

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“…4A and B). As previously reported [27], histone H3K4me3 and H3K9me3 were enriched on the maternal and paternal allele of Meg3 promoter, respectively (Fig. 4C).…”

Section: Resultssupporting

confidence: 88%

DNA methylation dynamics of a maternally methylated DMR in the mouse Dlk1–Dio3 domain

Zeng

Han

et al. 2014

FEBS Letters

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The mouse delta‐like homolog 1 and type III iodothyronine deiodinase (Dlk1–Dio3) imprinted domain contains three known paternally methylated differentially methylated regions (DMRs): intergenic DMR (IG‐DMR), maternally expressed 3‐DMR (Gtl2‐DMR), and Dlk1‐DMR. Here, we report the first maternally methylated DMR, CpG island 2 (CGI‐2), is located approximately 800 bp downstream of miR‐1188. CGI‐2 is highly methylated in sperm and oocytes, de‐methylated in pre‐implantation embryos, and differentially re‐methylated during post‐implantation development. CGI‐2, similarly to Gtl2‐DMR and Dlk1‐DMR, acquires differential methylation prior to embryonic day 7.5 (E7.5). Both H3K4me3 and H3K9me3 histone modifications are enriched at CGI‐2. Furthermore, CCCTC‐binding factor (CTCF) binds to both alleles of CGI‐2 in vivo. These results contribute to the investigation of imprinting regulation in this domain.

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“…4A and B). As previously reported [27], histone H3K4me3 and H3K9me3 were enriched on the maternal and paternal allele of Meg3 promoter, respectively (Fig. 4C).…”

Section: Resultssupporting

confidence: 88%

DNA methylation dynamics of a maternally methylated DMR in the mouse Dlk1–Dio3 domain

Zeng

Han

et al. 2014

FEBS Letters

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“…To demonstrate whether UHRF1 could regulate MEG3 expression in HCC, we altered the expression of UHRF1.The data showed the expression of UHRF1 was negatively associated with MEG3 expression. However, UHRF1 was never reported to be a regulatory factor of MEG3.Interestingly, we found that hypermethylation of MEG3 promoter, which may be responsible to the down‐regulation of MEG3, has been detected in many malignancies . Besides, UHRF1 was reported acting a crucial role in DNA methylation by recruiting DNMT1 to hemimethylated DNA during DNA replication .…”

Section: Discussionmentioning

confidence: 84%

The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma

Han

Tang

Zhe

et al. 2015

Molecular Carcinogenesis

132

122

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MEG3 as a tumor suppressor has been reported to be linked with pathogenesis of malignancies including hepatocellular carcinoma (HCC). However, the mechanism of MEG3 in HCC still remains unclear. In our study, the aberrant decreased level of MEG3 in 72 tumor tissues obtained from HCC patients and cell lines was examined by using real-time PCR. The inhibition affection in proliferation and inducing affection in apoptosis was further confirmed in vivo and vitro, we also demonstrated that MEG3 regulates HCC cell proliferation and apoptosis partially via the accumulation of p53. Besides, the hypermethylation of MEG3 in promoter region was identified by bisulfite sequencing while MEG3 increased with the inhibition of methylation. Subsequently, UHRF1, a new identified oncogene which is required for DNA methylation and recruits, was investigated. A negative correlation of MEG3 and UHRF1 expression was verified in primary HCC tissues. Down-regulation of UHRF1 induced MEG3 expression in HCC cell lines, which could be reversed by the up-regulation of UHRF1. In addition, up-regulation of MEG3 in HCC cells partially diminished the promotion of proliferation induced by UHRF1. Moreover, Kaplan-Meier analysis demonstrated that the patients with low expression of MEG3 indicated worse overall and relapse-free survivals compared with high expression of MEG3. Cox proportional hazards analyses showed that MEG3 expression was an independent prognostic factor for HCC patients. In conclusion, we demonstrated MEG3, acting as a potential biomarker in predicting the prognosis of HCC, was regulated by UHRF1 via recruiting DNMT1 and regulated p53 expression.

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“…There have been multiple efforts to dissect the functions of the maternallyexpressed lncRNAs in the Meg3-Rian-Mirg locus over the past decade (McMurray & Schmidt, 2012;Steshina et al, 2006;Takahashi et al, 2009;Zhou et al, 2010), but definitive results remain elusive. The difficulty is mainly attributable to two major hurdles; namely that 1) there are many DMRs that control imprinting status in upstream, promoter, and exon regions of Meg3, and 2) Meg3 might function in cis to regulate its imprinting status (Matsubara et al, 2015;Ogata & Kagami, 2016).…”

Section: Combinatorial and Individual Roles Of The Meg3-rian-mirg Lncmentioning

confidence: 99%

Dlk1-Dio3Locus-Derived LncRNAs Perpetuate Postmitotic Motor Neuron Cell Fate and Subtype Identity

Yen

Hsieh

et al. 2018

Preprint

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Identification of imprinting regulators at the Meg3 differentially methylated region

Cited by 24 publications

References 50 publications

DNA methylation dynamics of a maternally methylated DMR in the mouse Dlk1–Dio3 domain

DNA methylation dynamics of a maternally methylated DMR in the mouse Dlk1–Dio3 domain

The aberrant expression of MEG3 regulated by UHRF1 predicts the prognosis of hepatocellular carcinoma

Dlk1-Dio3Locus-Derived LncRNAs Perpetuate Postmitotic Motor Neuron Cell Fate and Subtype Identity

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