Maternally expressed gene 3 (MEG3): A tumor suppressor long non coding RNA

Ghafouri‐Fard, Soudeh; Taheri, Mohammad

doi:10.1016/j.biopha.2019.109129

Cited by 144 publications

(99 citation statements)

References 100 publications

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“…And the transcript variant 1 (homo, NR_002766.2) is the predominant transcript among the 15 distinct transcripts of MEG3. MEG3, a tumor suppressor, 50 had been found to involve in different biology progresses, such as cell cycle, 51 cell pyroptosis 52 and EMT 53 . Piccoli et al found that the level of MEG3 is decreased in cardiac fibrosis by microarray analysis 35 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

Zhan

Chang

Wang

et al. 2021

Environmental Toxicology

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Nickel oxide nanoparticles (NiO NPs) causes pulmonary fibrosis via activating transforming growth factor-β1 (TGF-β1) in rats, but its upstream regulatory mechanisms are unknown. This study aimed to explore the role of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in NiO NPs-induced collagen deposition. Male Wistar rats were intratracheally instilled with NiO NPs (0.015, 0.06, and 0.24 mg/kg b.w.) twice a week for 9 weeks. Human lung adenocarcinoma epithelial cells (A549 cells) were cultured with NiO NPs (25, 50, and 100 μg/ml) to establish collagen deposition model. We discovered that NiO NPs-induced rat pulmonary fibrosis was accompanied by the epithelial-mesenchymal transition (EMT) occurrence and MEG3 down-regulation in rat lung tissues. In cell collagen deposition model, NiO NPs also evoked EMT and decreased MEG3 expression in a dose-dependent manner in A549 cells. By overexpressing MEG3 in A549 cells, we found that MEG3 inhibited the level of TGF-β1, EMT process and collagen formation. Moreover, our data showed that SB431542 (TGF-β1 inhibitor) had an inhibitory effect on NiO NPs-induced EMT and collagen formation. Our results indicated that MEG3 inhibited NiO NPs-induced collagen deposition by regulating TGF-β1-mediated EMT process, which may provide some clues for insighting into the mechanisms of NiO NPs-induced pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

Zhan

Chang

Wang

et al. 2021

Environmental Toxicology

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“…The tumor suppressor MEG3 functions to inhibit tumor cell proliferation by regulating the expression of target genes of the tumor suppressor p53. [ 42 ] We subsequently constructed a ceRNA network based on DELs-miRNA and miRNA-DEGs pairs, which included 222 regulatory associations. The 2 DELs, MEG3, and C3orf35, were found to indirectly regulate the expression of key genes TTK, RRM2, and CDK1 by miRNAs (for example, miRNA-140-5p, [ 43 ] and miRNA-212-3p [ 44 ] ), that implied new clues on mechanisms of RB tumorigenesis and developing.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of multi-omics data identifying molecular biomarker candidates and epigenetically regulatory targets associated with retinoblastoma

Zeng¹,

He²,

Liu³

et al. 2020

Medicine

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Retinoblastoma (RB) is the commonest malignant tumor of the infant retina. Besides genetic changes, epigenetic events are also considered to implicate the occurrence of RB. This study aimed to identify significantly altered protein-coding genes, DNA methylation, microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and their molecular functions and pathways associated with RB, and investigate the epigenetically regulatory mechanism of DNA methylation modification and non-coding RNAs on key genes of RB via bioinformatics method. We obtained multi-omics data on protein-coding genes, DNA methylation, miRNAs, and lncRNAs from the Gene Expression Omnibus database. We identified differentially expressed genes (DEGs) using the Limma package in R, discerned their biological functions and pathways using enrichment analysis, and conducted the modular analysis based on protein-protein interaction network to identify hub genes of RB. Survival analyses based on The Cancer Genome Atlas clinical database were performed to analyze prognostic values of key genes of RB. Subsequently, we identified the differentially methylated genes, differentially expressed miRNAs (DEMs) and lncRNAs (DELs), and intersected them with key genes to analyze possible targets of the underlying epigenetic regulatory mechanisms. Finally, the ceRNA network of lncRNAs-miRNAs-mRNAs was constructed using Cytoscape. A total of 193 DEGs, 74 differentially methylated-DEGs (DM-DEGs), 45 DEMs, 5 DELs were identified. The molecular pathways of DEGs were enriched in cell cycle, p53 signaling pathway, and DNA replication. A total of 10 key genes were identified and found significantly associated with poor survival outcome based on survival analyses, including CDK1, BUB1, CCNB2, TOP2A, CCNB1, RRM2, KIF11, KIF20A, NDC80, and TTK. We further found that hub genes MCM6 and KIF14 were differentially methylated, key gene RRM2 was targeted by DEMs, and key genes TTK, RRM2, and CDK1 were indirectly regulated by DELs. Additionally, the ceRNA network with 222 regulatory associations was constructed to visualize the correlations between lncRNAs-miRNAs-mRNAs. This study presents an integrated bioinformatics analysis of genetic and epigenetic changes that may be associated with the development of RB. Findings may yield many new insights into the molecular biomarker candidates and epigenetically regulatory targets of RB.

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“…LncRNA MEG3-miRNA-mRNA: MEG3 is an imprinted gene and a tumor suppressive lncRNA. MEG3 is inversely related to tumorigenesis and plays an inhibitory role in many malignancies[ 92 ]. Acting as a ceRNA against miRNA is an important mechanism of action of MEG3 in HCC.…”

Section: Role Of Lncrnas As Cernas In Hccmentioning

confidence: 99%

Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma

Niu¹,

Wang²,

Dong³

et al. 2020

WJG

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Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are noncoding RNAs (ncRNAs) that occupy over 90% of the human genome, and their main function is to directly or indirectly regulate messenger RNA (mRNA) expression and participate in the tumorigenesis and progression of malignances. In particular, some lncRNAs can interact with miRNAs as competing endogenous RNAs (ceRNAs) to modulate mRNA expression. Accordingly, these RNA molecules are interrelated and coordinate to form a dynamic lncRNA-mediated ceRNA regulatory network. Mounting evidence has revealed that lncRNAs that act as ceRNAs are closely related to tumorigenesis. To date, numerous studies have established many different regulatory networks in hepatocellular carcinoma (HCC), and perturbations in these ceRNA interactions may result in the initiation and progression of HCC. Herein, we emphasize recent advances concerning the biological function of lncRNAs as ceRNAs in HCC, with the aim of elucidating the molecular mechanism underlying these HCC-related RNA molecules and providing novel insights into the diagnosis and treatment of HCC.

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Maternally expressed gene 3 (MEG3): A tumor suppressor long non coding RNA

Cited by 144 publications

References 100 publications

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

Bioinformatics analysis of multi-omics data identifying molecular biomarker candidates and epigenetically regulatory targets associated with retinoblastoma

Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma

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