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RNA-seq analysis of withdrawal of miR-155 hyperexpression in miR-155-addicted tumors

ABSTRACT: Overexpression of miR-155 in hematological tissue leads to the onset of lymphoma, and Tet-off shutdown of this overexpression reverses the disease phenotype in mir-155LSLtTA mice. This study compares the gene expression profiles of tumors with miR-155 overexpression and withdrawal. Examination of mRNA from 2 conditions: miR-155 overexpressing tumors and miR-155 overexpressing tumors from mice exposed to doxycycline (DOX) for 16hrs prior to harvest; samples in triplicate; tumors generated in flanks of nude mice by subcutaneous injection of splenic cells from diseased mir-155LSLtTA mice.

ORGANISM(S): Mus musculus

SUBMITTER: Christopher Cheng

PROVIDER: E-GEOD-61851 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MicroRNA silencing for cancer therapy targeted to the tumour microenvironment.

Cheng Christopher J CJ Bahal Raman R Babar Imran A IA Pincus Zachary Z Barrera Francisco F Liu Connie C Svoronos Alexander A Braddock Demetrios T DT Glazer Peter M PM Engelman Donald M DM Saltzman W Mark WM Slack Frank J FJ

Nature 20141117 7537

MicroRNAs are short non-coding RNAs expressed in different tissue and cell types that suppress the expression of target genes. As such, microRNAs are critical cogs in numerous biological processes, and dysregulated microRNA expression is correlated with many human diseases. Certain microRNAs, called oncomiRs, play a causal role in the onset and maintenance of cancer when overexpressed. Tumours that depend on these microRNAs are said to display oncomiR addiction. Some of the most effective antica ...[more]

PMID: 25409146

Similar Datasets

RNA-seq analysis of withdrawal of miR-155 hyperexpression in miR-155-addicted tumors

Project description:Overexpression of miR-155 in hematological tissue leads to the onset of lymphoma, and Tet-off shutdown of this overexpression reverses the disease phenotype in mir-155LSLtTA mice. This study compares the gene expression profiles of tumors with miR-155 overexpression and withdrawal.

2015-01-30 | GSE61851 | GEO

Mouse livers: control vs miR-155 transgenic mice

Project description:Transcriptional profiling of mouse livers comparing control mice with miR-155 transgenic mice that overexpression of miR-155 in the liver

2017-02-09 | GSE64255 | GEO

Expression analysis of eu-miR-155 transgenic mice B-cells.

Project description:miR-155 transgenic mice develop pre-B cell leukemia/lymphoma. Though some targets of miR-155 are known, understanding of the mechanism by which miR-155 overexpression drives malignant transformation is not known. MicroRNAs regulate multiple genes.

2012-12-03 | GSE30248 | GEO

Expression analysis of eu-miR-155 transgenic mice B-cells.

2012-12-03 | E-GEOD-30248 | biostudies-arrayexpress

Inhibition of the miR-155 target NIAM phenocopies the growth promoting effect of miR-155 in B-cell lymphoma [L1236]

Project description:Several studies have indicated an important role for miR-155 in the pathogenesis of B-cell lymphoma. Highly elevated levels of miR-155 were indeed observed in most B-cell lymphomas with the exception of Burkitt lymphoma (BL). However, the molecular mechanisms that underlie the oncogenic role of miR-155 in B-cell lymphoma are not well understood. To identify the miR-155 targets relevant for B-cell lymphoma, we performed RNA immunoprecipitation of Argonaute 2 in Hodgkin lymphoma (HL) cells upon miR-155 inhibition and in BL cells upon ectopic expression of miR-155. We identified 54 miR-155-specific target genes in BL cells and confirmed miR-155 targeting of DET1, NIAM, TRIM32, HOMEZ, PSIP1 and JARID2. Five of these targets are also regulated by endogenous miR-155 in HL cells. Both overexpression of miR-155 and inhibition of expression of the novel miR-155 target gene NIAM increased proliferation of BL cells. In primary B-cell lymphoma NIAM-positive cases have significant lower levels of miR-155 as compared to NIAM-negative cases, suggesting that NIAM is also regulated by miR-155 in primary B-cell lymphoma. Thus, our data indicate an oncogenic role for miR-155 in B-cell lymphoma which involves targeting the tumor suppressor NIAM.

2015-07-16 | GSE70937 | GEO

Inhibition of the miR-155 target NIAM phenocopies the growth promoting effect of miR-155 in B-cell lymphoma [ST486]

2015-02-20 | GSE64484 | GEO

Inhibition of the miR-155 target NIAM phenocopies the growth promoting effect of miR-155 in B-cell lymphoma [KM-H2]

2015-07-16 | GSE70938 | GEO

Transcriptional profiles of miR-155 overexpressing CD8T cells during chronic infection

Project description:Persistent viral infections and tumors drive development of exhausted T (TEX) cells. In these settings, TEX cells establish an important host-pathogen or host-tumor stalemate. However, TEX cells erode over time, leading to loss of pathogen or cancer containment. We identified microRNA (miR)-155 as a key regulator of sustained TEX cell responses during chronic lymphocytic choriomeningitis virus (LCMV) infection. Genetic deficiency of miR-155 ablated CD8 T cell responses during chronic infection. Conversely, enhanced miR-155 expression promoted expansion and long-term persistence of TEX cells. However, rather than strictly antagonizing exhaustion, miR-155 promoted a terminal TEX cell subset. Transcriptional profiling identified coordinated control of cell signaling and transcription factor pathways, including the key AP-1 family member Fosl2. Overexpression of Fosl2 reversed the miR-155 effects, identifying a link between miR-155 and the AP-1 transcriptional program in regulating TEX cells. Thus, we identify a mechanism of miR-155 regulation of TEX cells and a key role for Fosl2 in T cell exhaustion.

2018-05-16 | GSE114482 | GEO

Overexpression of miR-155 enhances B-cell lymphoma growth by targeting TBRG1

Project description:MYC regulates the expression of multiple microRNA (miRNA) genes and defines the Burkitt lymphoma (BL) miRNA signature. Here, we investigate the role of the MYC-regulated miRNAs by gain- and loss-of-function analysis. Overexpression of 5 miRNAs that were significantly downregulated by MYC resulted in strong (miR-150, miR-26a, miR-26b) and mild (miR-29a, let-7a) impaired cell growth. Overexpression of miR-155 increased proliferation of BL cells. By RNA immunoprecipitation of Argonaute 2 in BL cells with and without miR-155 we identified 54 miR-155 target genes. Using an shRNA approach we identified TBRG1 (NIAM1) as a miR-155 target gene that copied the miR-155-induced phenotype upon its inhibition. Analysis of TBRG1 protein expression and miR-155 levels in primary cases of B-cell lymphoma revealed that miR-155 levels are significantly lower in TBRG1 positive cases suggesting that TBRG1 is also regulated by miR-155 in primary B-cell lymphoma. Our data demonstrate that overexpression of individual MYC-repressed miRNAs has a strong suppressive effect on BL cell growth, whereas overexpression of miR-155 enhances B-cell lymphoma growth by targeting the tumor suppressor gene TBRG1. Gene expression profile was performed in ST486 Burkitt lymphoma cell line in 4 samples: ST486 EV (empty MXW-PGK-IRES-GFP vector) total cell lysate, ST486 EV Ago2-IP, ST486 miR-155 (ST486 with ectopic miR-155) total cell lysate, ST486 miR-155 Ago2-IP.

2015-02-20 | E-GEOD-64484 | biostudies-arrayexpress

Targeting AGTR1/NF-κB /CXCR4 axis by miR-155 attenuates oncogenesis in Glioblastoma

Project description:MiR-155 show conserved binding on the 3’UTR of AGTR1, subsequently confirmed by AGTR1-3’UTR-luciferase reporter assay. To determine the pathways regulated by miR-155, we overexpressed miR-155 in SNB19 glioblastoma cells using pLemiR lentiviral constructs. pLemiR vector, with turbo RFP (Open Biosystems) was used as control. Furthermore, stable miR-155 overexpressing GBM cells show a decrease in AGTR1-mediated cell proliferation, invasion, foci formation, anchorage-independent growth, Epithelial to Mesenchymal Transition and stemness.

2020-11-01 | GSE138737 | GEO

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