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Effect of MEG3 on p53 target genes in hepatoma cells

ABSTRACT: Maternally Expressed Gene 3 (MEG3) encodes a lncRNA which is suggested to function as a tumor suppressor. MEG3 functions as a tumor suppressor in hepatoma cells, whose action is mediated by interaction with p53 protein to activate p53-mediated transcriptional activity and influence the expression of partial p53 target genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69916 | GEO | 2015/06/17

SECONDARY ACCESSION(S): PRJNA287128

REPOSITORIES: GEO

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Effect of MEG3 on p53 target genes in hepatoma cells

Project description:Maternally Expressed Gene 3 (MEG3) encodes a lncRNA which is suggested to function as a tumor suppressor. MEG3 functions as a tumor suppressor in hepatoma cells, whose action is mediated by interaction with p53 protein to activate p53-mediated transcriptional activity and influence the expression of partial p53 target genes. Total RNA was isolated from hepatoma cells (HepG2 and SK-Hep-1) transfected with either control or MEG3 overexpression/knockdown constructs for global expression analysis.

2015-06-17 | E-GEOD-69916 | biostudies-arrayexpress

Expression data from different expressed genes(DEGs) in human esophageal squamous cell carcinoma(ESCC) EC109 cells transfected with empty lentiviral vector(Lv-NC) or lentiviral vector carrying MEG3(Lv-MEG3)

Project description:Maternally expressed gene 3 (MEG3), a member of lncRNAs, has tumor-suppressor properties and is downregulated in the majority of malignancies. MEG3 was found to suppress some sorts of tumors through regulating epithelial mesenchymal transformation,inducing cell cycle arrest,triggering apoptosis and so on. We used microarrays to investigate the possible regulatory mechanism of MEG3 in ESCC cell line.

2020-10-20 | GSE142036 | GEO

overexpression/knockdown MEG3 in C2C12 cell lines

Project description:MEG3 was known as a growth suppressor in tumor cells by activating p53. Besides, MEG3 could regulate transforming growth factor-β (TGF-β) signaling pathway, which is the key regulator of skeletal myogenesis and can enhance the proliferation of myogenic cells. Previous study also showed MEG3 was highly expressed in the paraxial mesoderm and probably regulated muscle development. To investigate the potential function of MEG3 in muscle development, we detected the expression levels of protein-coding genes after MEG3 over-expression or knockdown in C2C12 cell line using microarrays.

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Increased Expression of Angiogenic Genes in the Brains of Mouse Meg3-null Embryos

Project description:MEG3 (Maternally Expressed Gene 3) is a non-coding RNA that is highly expressed in the normal human brain and pituitary. Expression of MEG3 is lost in gonadotroph-derived clinically non-functioning pituitary adenomas. Meg3 knock-out mice were generated to identify targets and potential functions of this gene in embryonic development and tumorigenesis. Gene expression profiles were compared in the brains of Meg3-null embryos and wild-type litter-mate controls using microarray analysis. Microarray data were analyzed with GeneSifter which uses Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) classifications to identify signaling cascades and functional categories of interest within the data set. Differences were found in signaling pathways and ontologies related to angiogenesis between wild-type and knock-out embryos. Quantitative RT-PCR and histological staining showed increased expression of some VEGF pathway genes and increased cortical microvessel density in the knock-out embryos. These results are consistent with reported increases in VEGF signaling observed in human clinically non-functioning pituitary adenomas. In conclusion, Meg3 may play an important role in control of vascularization in the brain and may function as a tumor suppressor by preventing angiogenesis. Brains from 7 Meg3 knock-out and 6 wild-type E18.5 embryos from 5 litters. genotype: wild-type: 219_16 WT, 219_17 WT, 238_4 WT, 250_2 WT, 250_4 WT, 262_2 WT genotype: Meg3 knock-out: 148_15 KO, 219_12 KO, 238_1 KO, 238_5 KO, 250_1 KO, 250_3 KO, 262_1 KO biological replicate: 219_16 WT, 219_17 WT, 238_4 WT, 250_2 WT, 250_4 WT, 262_2 WT biological replicate: 148_15 KO, 219_12 KO, 238_1 KO, 238_5 KO, 250_1 KO, 250_3 KO, 262_1 KO

2010-12-17 | E-GEOD-18742 | biostudies-arrayexpress

Increased Expression of Angiogenic Genes in the Brains of Mouse Meg3-null Embryos

2010-12-17 | GSE18742 | GEO

Downregulation of LATS kinases alters p53 to promote cell migration

Project description:p53 is a pivotal tumor suppressor and a major barrier against cancer. We now report that silencing of the Hippo pathway tumor suppressors LATS1 and LATS2 in non-transformed mammary epithelial cells reduces p53 phosphorylation and increases its association with the p52 NF-κB subunit. Moreover, it partly shifts p53’s conformation and transcriptional output towards a state resembling cancer-associated p53 mutants, and endow p53 with the ability to promote cell migration. Notably, LATS1 and LATS2 are frequently downregulated in breast cancer; we propose that such downregulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator.

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ChIP-seq in MEG3+ and MEG3- hIPSCs

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2013-12-25 | E-GEOD-48516 | biostudies-arrayexpress

Expression profiling of Eµ-Myc-driven lymphomas using a reversible switchable p53 allele modeling early and late stage p53 inactivation.

Project description:For the most frequently inactivated tumor suppressor p53, genetic mouse models have demonstrated regression of p53-null tumors upon p53 reactivation. While this was shown in tumor models driven by p53 loss as the initiating lesion, many tumors initially develop in the presence of wild-type p53, acquire aberrations in the p53 pathway to bypass p53-mediated tumor suppression, and inactivate p53 itself only at later stages during metastatic progression or therapy. To explore the efficacy of p53 reactivation in this scenario, we used a reversibly switchable p53 (p53ERTAM) mouse allele to generate Eµ-Myc-driven lymphomas in the presence of active p53 and, after full lymphoma establishment, switched off p53 to model late-stage p53 inactivation.

2019-10-18 | E-MTAB-8015 | biostudies-arrayexpress

Expression data of GTSE1-knockdown hepatoma cell line Bel-7404

Project description:Liver cancer is the fourth deadliest cancer worldwide and is in lack of prognostic indicators. As a p53 inducible gene, GTSE1 (G2 and S phase-expressed-1) showed widely correlation with tumor progress and prognosis in clinical, while its potency as a prognosis indicator or molecular mechanism in regulating cell cycle remain little known. This study aimed to elucidate clinical values and potential functions of GTSE1 in liver cancer. In study of GTSE1 functions, Bel-7404 cell, a human hepatoma cell line, was induced GTSE1-knockdown using lentiviral-mediated RNAi and performed RNA microarray analysis.

2019-04-20 | GSE130083 | GEO

DBC1 regulates p53 stability via inhibition of CBP-dependent p53 polyubiquitination

Project description:The control of p53 protein stability is critical to its tumor suppressor functions. The CREB Binding Protein (CBP) transcriptional coactivator co-operates with MDM2 to maintain normally low physiologic p53 levels in cells via an exclusively cytoplasmic ‘E4’ polyubiquitination activity. Utilizing mass spectrometry to identify nuclear and cytoplasmic CBP interacting proteins that regulate compartmentalized CBP E4 activity, we identified Deleted in Breast Cancer 1 (DBC1) as a stoichiometric CBP-interacting protein that negatively regulates CBP–dependent p53 polyubiquitination, stabilizes p53, and augments p53-dependent apoptosis. TCGA analysis demonstrated that solid tumors often retain wild type p53 alleles in conjunction with DBC1 loss, supporting the hypothesis that DBC1 is selected for disruption during carcinogenesis as a surrogate for p53 functional loss. As DBC1 maintains p53 stability in the nucleus where p53 exerts its tumor suppressive transcriptional function, replacement of DBC1 functionality in DBC1-deleted tumors might also enhance p53 function and chemosensitivity for therapeutic benefit.

2019-11-13 | PXD012673 | Pride

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