CTCL and ATL cell lines, mir-150 transfected versus controls
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE49308 | GEO | 2013/07/30
SECONDARY ACCESSION(S): PRJNA213615
REPOSITORIES: GEO
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Project description:We examined the function of miR-150 in T-cell lymphomagenesis. We transfected GFP-control or GFP-miR-150 into several T-cell lymphoma lines and sought which genes were regulated by miR-150. To examine the function of miR-150 in T-cell lymphomagenesis, we first transfected GFP-control (Mock) or GFP-miR-150 into several T-cell lymphoma lines (ATN-1, HUT78, My-La, and HH). To detect genes commonly downregulated among these cells, we used the CodeLinkTM Human Whole Genome Bioarray platform with the criterion that the miR-150/GFP-control ratio must be <0.75 in all 3 CTCL lines.
2013-07-30 | E-GEOD-49308 | biostudies-arrayexpress
Project description:Human CD4+ Total memory cells (CD4+CD25-CD45RA-CCR7+/-) were activated for 5d with anti-CD3/anti-CD28 antibodies and transfected with biotinylated miR-150 mimic or biotinylated mimic negative control by Exiqon. After 24h cells were lysed and miRNA:mRNA complexes pulled-down with streptavidin agarose O/N at 4°C. RNA was then purified using TRI-reagent and RNA zymospin columns. Three independent donors were used for this experiment. Inputs were also sequenced. Total RNA was sequenced in single end mode. This experiment is assessing direct targets bound by miR-150-5p in human T cells.
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Project description:MicroRNAs are a major class of gene regulators in mammals. While numerous aspects of the immune systems are controlled by miRNAs, their precise role in the CD8+ T cell response remains unclear. In this report, we show that miR-150 is the most abundant miRNA expressed in CD8+ T cells and its expression is required for proper effector cell differentiation in response to acute and chronic pathogens. In the absence of miR-150, CD8+ T cells failed to both undergo robust expansion and differentiate into short-lived terminal effector cells. The lack of miR-150 also altered the effector CD8+ T cell transcriptome such that, despite activation, genes associated with naïve or memory cells were highly expressed. The deletion of miR-150 also reduced killing efficiency of CD8+ T cells. These results uncover a cell-intrinsic role for miR-150 in the regulation of CD8+ T cell effector fate and function.
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Project description:miR-150 Pulldown-sequencing data
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Project description:In Burkitt lymphoma (BL), a network consisting of MYC, MYC-repressed miR-150, known miR-150 target MYB and two novel targets of miR-150, ZDHHC11 and ZDHHC11B, has been established. This network plays an important role on the growth of BL cells. Here, we confirmed that MYB, ZDHHC11 and ZDHHC11B are targeted by miR-150 in Hodgkin lymphoma (HL) cell lines too.
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Project description:This study report that miR-150, a key hematopoietic regulatory microRNA (miRNA) and one of the most downregulated miRNAs in MLL-associated leukemias, acts as a tumor suppressor to block the leukemogenic potency of leukemic stem cells. When expression of miR-150 was restored, a significantly suppressed leukemic stem cell potency of MLL-AF9 cells was observed both in vivo and in vitro. To investigate the tumor suppressive function of miR-150 in MLL-AF9 cells, we isolated three batches of MLL-AF9 cells infected with MDH empty vector or MDH-miR-150 expression retrovirus. Total RNA were extracted and applied for Agilent array analysis. Gene profiling analysis demonstrated that elevated miR-150 altered various aspects of gene expression patterns in MLL-AF9 cells, including stem cell signatures, cancer pathways, and cell survival.
2011-07-20 | GSE30771 | GEO
Project description:The oncogenic transcription factor MYC regulates expression of protein-coding genes, microRNAs and long non-coding RNAs. Here we show that overexpression of the MYC-repressed miR-150 severely impaired growth of Burkitt lymphoma (BL) cells. AGO2-RIP-Chip revealed two novel miR-150 targets, ZDHHC11 and ZDHHC11B, as the two most enriched genes, followed by MYB, a known miR-150 target. ZDHHC11 and ZDHHC11B encode both protein-coding and non-coding transcripts and contain a strikingly high number of miR-150 binding sites, i.e. 18 and 62, respectively. Effective targeting of ZDHHC11 and ZDHHC11B by miR-150 was confirmed by luciferase assay and for the ZDHHC11 protein by Western blot. Furthermore, we identified a circular ZDHHC11 transcript which contains the miR-150 binding site region and interacts strongly with miR-150. Knockdown of both MYB and ZDHHC11/ZDHHC11B significantly impaired growth of BL cells. Moreover, downregulation of ZDHHC11/ZDHHC11B also resulted in reduced MYB levels in BL cells. Together, our results demonstrate that elevated levels of MYB required for the high proliferative state of BL cells are ensured in two ways. First, MYC represses the tumor suppressor miR-150, which prevents its inhibitory effects on MYB expression. Second, the novel miR-150 targets ZDHHC11 and ZDHHC11B are required for maintaining high MYB levels in BL cells.
2017-03-24 | GSE86432 | GEO
Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific miR-150 conditional knockout KO (cKO) mice were performed to identify novel miR-150 targets in the heart.
2021-08-18 | GSE177057 | GEO
Project description:The objective of these experiments is to identify novel direct and indirect targets of miR-150-5p in breast cancer cell lines. The goal is that these will give direction as to what targets or pathways may be contributing to the reduced growth observed in these cell lines upon restoration of miR-150-5p. A therapy directed towards one or more critical subtype-specific targets could be developed as a therapeutic for breast cancer patients. Using has-miR-150-5p mirVana miRNA mimic (Ambion, 4464066), miR-150-5p was restored to a triple negative breast cancer cell line, BT-549.
2017-01-01 | GSE87589 | GEO
Project description:This study report that miR-150, a key hematopoietic regulatory microRNA (miRNA) and one of the most downregulated miRNAs in MLL-associated leukemias, acts as a tumor suppressor to block the leukemogenic potency of leukemic stem cells. When expression of miR-150 was restored, a significantly suppressed leukemic stem cell potency of MLL-AF9 cells was observed both in vivo and in vitro. To investigate the tumor suppressive function of miR-150 in MLL-AF9 cells, we isolated three batches of MLL-AF9 cells infected with MDH empty vector or MDH-miR-150 expression retrovirus. Total RNA were extracted and applied for Agilent array analysis. Gene profiling analysis demonstrated that elevated miR-150 altered various aspects of gene expression patterns in MLL-AF9 cells, including stem cell signatures, cancer pathways, and cell survival. miR-150-MLL-AF9 and MDH-MLL-AF9 isolated cells were compared for gene expression patterns. Triplicates using three batches of FACS sorted cells were compared in pairs on the array. MDH-MLL-AF9 samples were labeld with Cy3 and miR-150-MLL-AF9 samples were labled with Cy5.
2011-07-19 | E-GEOD-30771 | biostudies-arrayexpress