MEG3: a novel long noncoding potentially tumour-suppressing RNA in meningiomas

Balik, Vladimír; Srovnal, Josef; Šulla, I; Kalita, Ondřej; Foltánová, Tatiana; Vaverka, Miroslav; Hrabálek, Lumir; Hajdúch, Marián

doi:10.1007/s11060-012-1038-6

Cited by 109 publications

(75 citation statements)

References 69 publications

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“…We found that two lncRNAs - MEG3 (Maternally Expressed Gene 3) and KIAA0125 - compete for the role of the first hub and regulate the expression of the almost totality of the mRNAs in the cancer-MMI-network, by antagonizing mir-379 and mir-150, respectively (Additional file 5: Tables S5 and S10). Of note, MEG3 was recently suggested to play a significant role as a novel tumor suppressor lncRNA in several human cancers and evidence of its association with tumorigenesis is growing every day [41-43]. Functional annotation enrichment analysis of nodes in this larger sub-network clearly points to immune system-related functions (Additional file 12: Figure S3 and Additional file 13: Table S11).…”

Section: Resultsmentioning

confidence: 96%

Computational analysis identifies a sponge interaction network between long non-coding RNAs and messenger RNAs in human breast cancer

2014

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BackgroundNon-coding RNAs (ncRNAs) are emerging as key regulators of many cellular processes in both physiological and pathological states. Moreover, the constant discovery of new non-coding RNA species suggests that the study of their complex functions is still in its very early stages. This variegated class of RNA species encompasses the well-known microRNAs (miRNAs) and the most recently acknowledged long non-coding RNAs (lncRNAs). Interestingly, in the last couple of years, a few studies have shown that some lncRNAs can act as miRNA sponges, i.e. as competing endogenous RNAs (ceRNAs), able to reduce the amount of miRNAs available to target messenger RNAs (mRNAs).ResultsWe propose a computational approach to explore the ability of lncRNAs to act as ceRNAs by protecting mRNAs from miRNA repression. A seed match analysis was performed to validate the underlying regression model. We built normal and cancer networks of miRNA-mediated sponge interactions (MMI-networks) using breast cancer expression data provided by The Cancer Genome Atlas.ConclusionsOur study highlights a marked rewiring in the ceRNA program between normal and pathological breast tissue, documented by its “on/off” switch from normal to cancer, and vice-versa. This mutually exclusive activation confers an interesting character to ceRNAs as potential oncosuppressive, or oncogenic, protagonists in cancer. At the heart of this phenomenon is the lncRNA PVT1, as illustrated by both the width of its antagonist mRNAs in normal-MMI-network, and the relevance of the latter in breast cancer. Interestingly, PVT1 revealed a net binding preference towards the mir-200 family as the bone of contention with its rival mRNAs.

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Section: Resultsmentioning

confidence: 96%

Computational analysis identifies a sponge interaction network between long non-coding RNAs and messenger RNAs in human breast cancer

2014

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“…For example, the 21 kb lncRNA MEG3 was up-regulated in fetal heart and is a known tumor suppressor. 27 A second 382 bp lncRNA, BCYRN1, was up-regulated in adult heart and has been reported to be up-regulated and targeted by c-MYC in non-small-cell lung cancer. 28 …”

Section: Resultsmentioning

confidence: 99%

Systematic Characterization of Long Noncoding RNAs Reveals the Contrasting Coordination of Cis - and Trans -Molecular Regulation in Human Fetal and Adult Hearts

Wilson

et al. 2016

Circ Cardiovasc Genet

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Background The molecular regulation of heart development is regulated by cis- and trans-factors acting on the genome and epigenome. As a class of important regulatory RNAs, the role of long non-coding RNAs (lncRNAs) in human heart development is still poorly understood. Furthermore, factors that interact with lncRNAs in this process are not well characterized. Methods and Results Utilizing RNA sequencing, we systematically define the contrasting lncRNA expression patterns between fetal and adult heart. We report that lncRNAs up-regulated in adult versus fetal heart have different sequence features and distributions. For example, the adult heart expresses more sense lncRNAs compared to fetal heart. We also report the co-expression of lncRNAs and neighboring coding genes that have important functions in heart development. Importantly, the regulation of lncRNA expression during fetal to adult heart development appears to be due in part to the coordination of specific developmental epigenetic modifications such as H3K4me1 and H3k4me3. The expression of promoter-associated lncRNAs in adult and fetal heart also appears to be related to these epigenetic states. Finally, transcription factor binding analysis suggests that lncRNAs are directly regulating cardiac gene expression during development. Conclusions We provide a systematic analysis of lncRNA control of heart development that gives clues to the roles that specific lncRNAs play in fetal and adult hearts.

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“…Meg3 is an imprinted gene, and its transcript is a noncoding RNA highly expressed in the developing and adult mouse neocortex, hypothalamus, hippocampus, and amygdala (Balik et al, 2013). The human homolog of the mouse Meg3 gene, MEG3 , is found to express in the brain and pituitary (Gejman et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Identification of sexually dimorphic genes in the neonatal mouse cortex and hippocampus

et al. 2014

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The cerebral cortex and hippocampus are important for the control of cognitive functions and social behaviors, many of which are sexually dimorphic and tightly regulated by gonadal steroid hormones via activation of their respective nuclear receptors. As different levels of sex steroid hormones are present between the sexes during early development and their receptors act as transcription factors to regulate gene expression, we hypothesize that sexually dimorphic gene expression in the developing mouse cortex and hippocampus might result in sex differences in brain structures and neural circuits governing distinct behaviors between the sexes as adults. To test our hypothesis, we used gene expression microarrays to identify 90 candidate genes differentially expressed in the neonatal cortex/hippocampus between male and female mice, including 55 male-biased and 35 female-biased genes. Among these genes, sexually dimorphic expression of eight sex chromosome genes was confirmed by reverse transcription with quantitative PCR (RT-qPCR), including three located on the X chromosome (Xist, Eif2s3x, and Kdm6a), three on the Y chromosome (Ddx3y, Eif2s3y, and Kdm5d), and two in the pseudoautosomal region of the X and Y chromosomes (Erdr1 and Mid1). In addition, five autosomal genes (Cd151, Dab2, Klk8, Meg3, and Prkdc) were also validated for their sexually dimorphic expression in the neonatal mouse cortex/hippocampus. Gene Ontology annotation analysis suggests that many of these sexually dimorphic genes are involved in histone modifications, cell proliferation/death, androgen/estrogen signaling pathways, and synaptic organization, and these biological processes have been implicated in differential neural development, cognitive function, and neurological diseases between the sexes.

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MEG3: a novel long noncoding potentially tumour-suppressing RNA in meningiomas

Cited by 109 publications

References 69 publications

Computational analysis identifies a sponge interaction network between long non-coding RNAs and messenger RNAs in human breast cancer

Computational analysis identifies a sponge interaction network between long non-coding RNAs and messenger RNAs in human breast cancer

Systematic Characterization of Long Noncoding RNAs Reveals the Contrasting Coordination of Cis - and Trans -Molecular Regulation in Human Fetal and Adult Hearts

Identification of sexually dimorphic genes in the neonatal mouse cortex and hippocampus

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