49a825c3-18bb-44ea-a4bc-f1afcc86c4ad - samples
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ABSTRACT:
PROVIDER: EGAD00001008480 | EGA |
REPOSITORIES: EGA
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Project description:Gain of chromosome arm 13q is one of the most prevalent DNA copy number alterations associated with colorectal adenoma-to-carcinoma progression. The oncogenic miR-17-92 cluster, located at 13q, was found to be overexpressed in colorectal cancer and in adenomas harboring 13q gain. However, to what extent overexpression of this group of microRNAs actually drives progression to cancer remains to be resolved. Therefore, we aimed to clarify the role of miR-17-92 cluster in the progression from colorectal adenoma to carcinoma.
In human colorectal adenoma organoids without 13q gain, the miR-17-92 cluster was overexpressed and downstream effects on mRNA expression investigated, along with functional effects in vitro and in vivo.
Comparison of mRNA sequencing results of organoids overexpressing miR-17-92 and cultures transduced with control vector, revealed a miR-17-92 expression signature. This signature appeared to be enriched in an independent series of colorectal cancers and adenomas tissues with 13q gain, confirming that miR-17-92 expression is associated with malignant progression. However, an increase in proliferation rate was not observed in miR-17-92 overexpressing adenoma organoids in vitro. In addition, subcutaneous injection of these organoids in immunodeficient mice was insufficient to cause tumor outgrowth.
Transfecting miR-17-92 cluster in human colon adenoma organoids induces an expression signature that proved to be enriched in both adenomas with 13q gain and in colorectal cancers, supporting its role as a driver of 13q gain. However, overexpression of miR-17-92 alone is not sufficient to transform colorectal adenoma cells into a malignant phenotype.
| EGAS00001005949 | EGA
Project description:miR-17 from the miR-17-92 cluster regulate activation-induced cell death in T cells and modulate inducible regulatory T cell differentiation. We used microarrays to detail the global program of gene expression modulated by miR-17 and aim to identify the potential targets of miR-17. CD4 T cells from wild type or miR-17-92 deficient mice were activated and transduced with empty vector or that overexpressing miR-17. Potential targets of miR-17 should be upregulated in miR-17-92 deficient CD4 T cells compared to wild type CD4 T cells, and downregulated when miR-17 were reintroduced into the miR-17-92 deficient T cells.
2011-09-30 | E-GEOD-32533 | biostudies-arrayexpress
Project description:Neural stem/progenitor cells were isolated from the lateral ventricle wall of 4-6 week-old CD1 mice and grown as neurospheres under low density culture conditions. Test cells were transduced with bicistronic retroviral constructs for the over-expression of Bmi1 together with eGFP, and control cells were transduced with an empty vector construct expressing eGFP only. To identify genes, which are regulated by BMI1 in neural stem/progenitor cells, the gene expression profiles of neurosphere cells over-expressing Bmi1 were compared empty vector control cells using Affymetrix Gene mouse ST1.0 arrays 3 independent Bmi1-overexpressing neurosphere cultures (test samples) were compared to 3 independent empty vector neurosphere cultures (control samples).
2016-06-01 | E-GEOD-70451 | biostudies-arrayexpress
Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the mammary epithelial cells MCF10A overexpressing human HER2 and HER3 and grown in 3D cultures for 15 days in the presence or absence of SHP2. The human mammary epithelial cells MCF10A were transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were grown in 3D cultures, and the knockdown of SHP2 was induced for 15 days. RNA was extracted for gene expression analysis.
2011-12-20 | E-GEOD-34524 | biostudies-arrayexpress
Project description:Global mRNA expression profiling of HCT116 cells overexpressing miR30a-5p were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Two different sources of RNA were analyzed: 1.) HCT116 colon cancer cells overexpressing human mir-30a-5p together with a sponge vector expressing binding sites for the antisense sequence of sh30a-5p vector construct to compete out possible miRNAs derived from the anti-guide strand of this vector. 2.) HCT116 colon cancer cells expressing control vector (pLKO.1-LV) and the sponge vector described above.
2012-03-08 | GSE29921 | GEO
Project description:Hematopoietic stem/progenitor cells (HS/PCs) were transduced with lentiviral vectors overexpressing OFP and either miR-511-3p or a control, mutated miRNA sequence (miR-511-3p-mut). The transduced HS/PCs were then transplanted in recipient C57BL/6 mice. Tumors (Lewis lung carcinomas, LLC) were injected s.c. 4 weeks after HS/PC transplant. Lentiviral vector-transduced (OFP+), tumor-associated macrophages (TAMs) were isolated 4 weeks after LLC injection by fluorescence-activated cell sorting. Gene expression profiles of TAMs overexpressing either miR-511-3p or miR-511-3p-mut were obtained from 3 independent biological samples/each. Gene expression profiles of miRNA-overexpressing TAMs were then compared with the gene expression profiles of wild-type TAMs isolated from LLCs grown in nontransplanted C57BL/6 mice; the latter TAMs were subfractioned into MRC1+CD11c(low) or CD11c+MRC1(low) subsets before RNA isolation and analysis. Comparison of gene expression profiles of TAMs revealed that miR-511-3p overexpression tunes down the expression of multiple genes that are classically upregulated in protumoral MRC1+CD11c(low) TAMs.
2012-04-01 | GSE34903 | GEO
Project description:miR-101 has been reported as a tumor suppressor in several types of cancer. However, its role in AML is still unknown. In this study, we restored the expression of miR-101 in MLL-AF9 transduced LSK cells by introducing a retroviral miR-101 expression vector. To identify miR-101-regulated gene expression, we performed genome-wide gene expression analysis on GFP+ MLL-AF9-transduced LSK cells overexpressing miR-101 versus control vector. Our gene expression analysis and subsequent functional studies demonstrate that enforced expression of miR-101 has antitumor effects on the development of MLL-rearranged AML. Each group has 3 samples.
2019-07-03 | E-MTAB-7344 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) have emerged as novel cancer genes. In particular, the 17~92 cluster of miRNAs is highly expressed in haematopoietic cancers and promotes lymphomagenesis in vivo1,2. Clinical use of these findings hinges on isolating the oncogenic activity within the 17~92 cluster and defining its relevant target genes. Here we show that miR-19 is sufficient to promote leukaemogenesis in Notch1 induced T-cell lymphoblastic leukaemia (T-ALL) in vivo. Consistent with the pathogenic importance of this interaction, we report a novel translocation targeting the 17~92 miRNA cluster coinciding with a second rearrangement that activates Notch1 in T-ALL. To identify the miR-19 targets responsible for its oncogenic action, we conducted a large-scale short-hairpin RNA (shRNA) screen for genes whose knockdown could phenocopy miR-19. Strikingly, the results of this screen were enriched for miR-19 target genes, and included Bim (Bcl2L11)1,3, AMP-activated kinase (Prkaa1), and the tumour suppressor phosphatases Pten and PP2A (Ppp2r5e). Hence, an unbiased, functional genomics approach reveals a coordinate clamp down on several regulators of PI3K-related survival signals by the leukaemogenic miR-19. Gene expression data revealing differences in gene expression between parental FL5-12 cells transduced with Vector and miR-19 expressing FL5-12 cells
2010-03-03 | E-GEOD-20097 | biostudies-arrayexpress
Project description:To unravel the molecular mechanism underlying miR-17∼92 costimulatory function, we performed RNA-seq on CD4+ T cells from mice lacking miR-17∼92 in T cell, wildtype mice and mice overexpressing miR-17∼92 in T cells, in naïve state or activated vitro for 24h and 48h.
2022-09-08 | GSE140525 | GEO
Project description:Lentiviral constructs expressing candidate tumoure suppressor genes were transduced into 697 cells. Of the candidates FOXO3, two isoforms of PRDM1 (⍺ and β) suppressed growth in-vitro and in-vivo. To indentify tumour suppressor mechanisms we extracted RNA from triplicate 697 cultures four days after transduced with empty vector (SIN-SIEW) or constructs expressing FOXO3, PRDM1⍺ or PRDM1β. Approximately 90 million 100bp paired-end reads were generated per sample by illumina sequencing.
2022-10-01 | GSE193347 | GEO