Analysis of Hepatoblastoma and normal fetal liver miRNA profiles and HepaRG cells that ectopically express miR-371-3 cluster
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE21085 | GEO | 2012/12/13
SECONDARY ACCESSION(S): PRJNA126699
REPOSITORIES: GEO
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2012-12-13 | E-GEOD-21085 | biostudies-arrayexpress
Project description:the immoratlized hepatic cell line HepaRG was transduced with a retroviral vector containing the miR-371-3 cluster. As a control, transduction was performed with the empty vector. Transcriptome analysis was performed by using the Affymetrix whole-transcript human gene 1.0 ST array. Each condition was analyzed in triplicate
2012-12-31 | GSE21080 | GEO
Project description:the immoratlized hepatic cell line HepaRG was transduced with a retroviral vector containing the miR-371-3 cluster. As a control, transduction was performed with the empty vector. Transcriptome analysis was performed by using the Affymetrix whole-transcript human gene 1.0 ST array. Each condition was analyzed in triplicate hierarchical unsupervised clustering of HB samples according to their miRNA expression profile identifies 2 tumor subgroups associated with different degree of differentiation, proliferation rate and invasive phenotype. As subset of these tumors is used as training set to build a mir classifier. When the signature is applied to an independent test set, an independent series of HB is classified patients into two groups associated with the clinical features identified in the first set of patients.
2012-12-31 | E-GEOD-21080 | biostudies-arrayexpress
Project description:A family of vertebrate-specific microRNAs called the ESCC microRNAs regulates proliferation and differentiation of embryonic stem cells. The ESCC microRNAs arise from two genetic loci in mammals, the miR-290/miR-371 and miR-302 loci. While the miR-302 locus is found broadly among vertebrates, the miR-290/miR-371 locus is unique to eutherian species, suggesting a role in placental development. Here, we evaluate that role. A knockin reporter for the mouse miR-290 gene is expressed throughout the embryo until gastrulation, at which time it becomes specifically expressed in extraembryonic tissues and the germline. In the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed until birth. Deletion of the miR-290 gene results in reduced trophoblast progenitor cell proliferation and a reduced DNA content in endoreduplicating trophoblast giant cells. A reduction in placental size precedes a reduction in fetal size and prenatal death of most knockout embryos. The vascular labyrinth shows disorganization with thickening of the barrier between maternal and fetal blood associated with reduced diffusion of a radioactive tracer. Multiple mRNA targets of the cluster miRNAs are upregulated. Together, these data uncover a critical function for the miR-290 in the regulation of a network of genes required for normal placental development, suggesting a central role for this microRNA cluster in the evolution of eutherian species.
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Project description:Oral squamous cell carcinoma (OSCC) is among the leading causes of cancer-associated deaths worldwide. Family members in miR-371/372/373 miRNA cluster, which is localized at human chromosome 19q13.4, are co-expressed in both human stem cells and malignancies. The individual miRNA in this cluster are also involved in modulating the pathogenesis of malignancies as either oncogenes or suppressors. The 19q13 region is frequently gained in head and neck cancers. High expression of miR-372 and miR-373 are survival predictors for OSCC. However, the role of the miR-371/372/373 cluster in oral carcinogenesis remains to be fully investigated. We use the clustered, regularly interspaced, short palindromic repeats (CRISPR)-Cas9 system to establish OSCC cell subclones that had the miR-371/372/373 cluster deleted. In addition, further subclones were established that had the promoter of this cluster deleted. Concordant silencing in SAS cells of miR-371/372/373 decreased oncogenic potential, increased cisplatin sensitivity, activated p53, and upregulated the expression of Bad and DKK1. We also employed the CRISPR/dCas9 synergistic activation mediator system, which allowed robust transcriptional activation of the whole miR-371/372/373 cistron. Upregulation of endogenous miR-371/372/372 expression increased both oncogenicity and drug resistance. These were accompanied by a slight activation of AKT, β-catenin, and Src. This study identifies the oncogenic role of the miR-371/372/373 cluster in OSCC. Using CRISPR based strategy can be a powerful paradigm that will provide mechanistic insights into miRNA cluster functionality, which will also likely help the development of targeting options for malignancies.
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Project description:Forty-nine hepatoblastoma (HB) tumor specimens were profiled on a microarray containing 250human miRNA, in order to identify miR classifiers that could discriminate HBs with diverse prognosis, and to get insight on the functional mechanisms in which miRNAs are involved. Hierarchical unsupervised clustering of HB samples according to their miRNA expression profile identifies 2 tumor subgroups associated with different degree of differentiation, proliferation rate and invasive phenotype. As subset of these tumors is used as training set to build a mir classifier. When the signature is applied to an independent test set, an independent series of HB is classified patients into two groups associated with the clinical features identified in the first set of patients.
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Project description:Chromatin architecture and dynamics are regulated by various histone and non-histone proteins. The matrix attachment region binding proteins (MARBPs) play a central role in chromatin organization and function through numerous regulatory proteins. In the present study, we demonstrate that nuclear matrix protein SMAR1 orchestrates global gene regulation as determined by massively parallel ChIP-sequencing. The study revealed that SMAR1 binds to T(C/G) repeat and targets genes involved in diverse biological pathways. We observe that SMAR1 binds and targets distinctly different genes based on the availability of p53. Our data suggest that SMAR1 binds and regulates one of the imperative microRNA clusters in cancer and metastasis, miR-371-373. It negatively regulates miR-371-373 transcription as confirmed by SMAR1 overexpression and knockdown studies. Further, deletion studies indicate that a ~200?bp region in the miR-371-373 promoter is necessary for SMAR1 binding and transcriptional repression. Recruitment of HDAC1/mSin3A complex by SMAR1, concomitant with alteration of histone marks results in downregulation of the miRNA cluster. The regulation of miR-371-373 by SMAR1 inhibits breast cancer tumorigenesis and metastasis as determined by in vivo experiments. Overall, our study highlights the binding of SMAR1 to T(C/G) repeat and its role in cancer through miR-371-373.
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