Ontology highlight
ABSTRACT:
PROVIDER: PRJNA118239 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To identify differentially expressed human and viral miRNAs across a panel of B-cell lines, including several primary effusion lymphomas (PEL). Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposi’s Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkitt’s lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression.
2015-12-05 | GSE18437 | GEO
Project description:To identify differentially expressed human and viral miRNAs across a panel of B-cell lines, including several primary effusion lymphomas (PEL). Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposiâs Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkittâs lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression. miRNA expression profiling of a panel of 25 B-cell line samples.
2015-12-05 | E-GEOD-18437 | biostudies-arrayexpress
Project description:1) To identify changes in gene expression upon over-expression of hsa-miR-221 in JSC1 cells. 2) To identify human miRNA targets expressed in a panel of B-cell lines. Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposi’s Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkitt’s lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression.
2015-12-05 | GSE18438 | GEO
Project description:1) To identify changes in gene expression upon over-expression of hsa-miR-221 in JSC1 cells. 2) To identify human miRNA targets expressed in a panel of B-cell lines. Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposiâs Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkittâs lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression. The dataset comes in two parts. 1) 6 JSC1 samples: 2 with miR-221 lentiviral vector, 2 without and 2 with K5 short hairpin RNA as control. 2) A panel of 14 B-cell line samples. Each of the 20 samples was Cy5 labelled and run with Cy3-labelled Stratagene reference RNA.
2015-12-05 | E-GEOD-18438 | biostudies-arrayexpress
Project description:We profiled miRNA expression in tissue samples (104 HCC, 90 adjacent cirrhotic livers, 21 normal livers) as well as in 35 HCC cell lines. A set of 12 miRNAs (including miR-21, miR-221/222, miR-34a, miR-519a, miR-93,miR-96, and let-7c) was linked to disease progression from normal liver through cirrhosis to full-blown HCC. miR-221/222, the most upregulated miRNAs in tumor samples, are shown to target the CDK inhibitor p27 and to enhance cell growth in vitro. Conversely, these activities can be efficiently inhibited by an antagomiR specific for miR-221. In addition, we show, using a mouse model of liver cancer, that miR-221 overexpression stimulates growth of tumorigenic murine hepatic progenitor cells.
2009-12-08 | E-TABM-866 | biostudies-arrayexpress
Project description:Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis.
2012-02-28 | GSE35078 | GEO
Project description:MicroRNAs (miRNAs) constitute fine tuners of gene expression and are implicated in a variety of diseases spanning from inflammation to cancer. miRNA expression is deregulated in rheumatoid arthritis (RA), however, their specific role in key arthritogenic cells such as the synovial fibroblast (SF) remains elusive. We have shown in the past that the expression of the miR-221/222 cluster is upregulated in RA SFs. Here, we demonstrate that miR-221/222 activation is downstream of major inflammatory cytokines, such as TNF and IL-1β, which promote miR-221/222 expression independently. miR-221/222 expression in SFs from the huTNFtg mouse model of arthritis correlates with disease progression. Targeted transgenic overexpression of miR-221/222 in SFs of the huTNFtg mouse model led to further expansion of synovial fibroblasts and disease exacerbation. miR-221/222 overexpression altered the transcriptional profile of SFs igniting pathways involved in cell cycle progression and ECM regulation. Validated targets of miR-221/222 included p27 and p57 cell cycle inhibitors, as well as Smarca1 (a chromatin remodeling component). In contrast, complete genetic ablation of miR-221/222 in arthritic mice led to decreased proliferation of fibroblasts, reduced synovial expansion and attenuated disease. scATAC-seq data analysis revealed increased miR-221/222 gene activity in the pathogenic and activated clusters of the intermediate and lining compartment. Taken together, our results establish an SF-specific pathogenic role of the miR-221/222 cluster in arthritis and suggest that its therapeutic targeting in specific subpopulations should inform the design of novel fibroblast-targeted therapies for human disease.
2022-12-16 | GSE210887 | GEO
Project description:Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis. Identification of endothelial-expressed microRNA from FACS-isolated zebrafish endothelial cells.
2012-02-28 | E-GEOD-35078 | biostudies-arrayexpress
Project description:Cell differentiation involves profound changes in global gene expression that often have to occur in coordination with cell cycle exit. Because cyclin-dependent kinase inhibitor p27 reportedly regulates proliferation of neural progenitor cells in the subependymal neurogenic niche of the adult mouse brain, but can also have effects on gene expression, we decided to molecularly analyze its role in adult neurogenesis and oligodendrogenesis. At the cell level, we show that p27 restricts residual cyclin-dependent kinase activity after mitogen withdrawal to antagonize cycling, but is not essential for cell cycle exit. Contrasting gene expression with chromatin accessibility, we find that p27 is coincidentally necessary to globally repress many genes involved in the transit from multipotentiality to differentiation, including those coding for neural progenitor transcription factors SOX2, OLIG2, and ASCL1. Our data reveal both direct association of p27 with regulatory sequences in the three genes and an additional hierarchical relationship where p27 repression of the Sox2 gene leads to reduced levels of SOX2-downstream targets Olig2 and Ascl1. In vivo, p27 is also required for the regulation of the proper level of SOX2 necessary for neuroblasts and oligodendroglial progenitor cells to timely exit cell cycle in a lineage-dependent manner.
2023-01-09 | GSE196285 | GEO
Project description:MiR-221 overexpression leads to activation of apoptosis, growth arrest and reduced invasivness in PCa cells. Interaction of miR-221 with potential target genes was analyzed by a genome wide expression profiling.. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real Time RT-PCR assay (IRF1, IRF2 SOCS3, STAT1), and Western Blotting. In total, 282 genes were upregulated and 64 downregulated based on a more than 2-fold difference to untransfected PC-3 cells. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, tumorigenesis and inflammation. We confirmed dysregulation of IRF-2 SOCS3, STAT1,IRF9. These results indicate that miR-221 overexpression might lead to activation of the JAK/STAT pathway and downregulation of miR-221 might contribute to tumorigenesis in PCa cells. pre-miR-221 transfected PC-3 cells vs unstimulated control cells - total samples analysed are 4.
2014-03-27 | E-GEOD-45627 | biostudies-arrayexpress