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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells

ABSTRACT: Transcriptional profiling of breast cancer cells comparing LNA-control transfected cells with cells transfected with LNA-antimiR-21.We searched for miR-21 targets by systematic screening of mRNA profiling of LNA-antimiR-21 transfected MCF-7 cells and MDA-MB-231 cells. Two-condition experiment, LNA-antimiR-21 Transfected vs. LNA-control Transfected MCF-7 cells. One replicate per array.

ORGANISM(S): Homo sapiens

SUBMITTER: Yan Zhang

PROVIDER: E-GEOD-20627 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells

Project description:Transcriptional profiling of breast cancer cells comparing LNA-control transfected cells with cells transfected with LNA-antimiR-21.We searched for miR-21 targets by systematic screening of mRNA profiling of LNA-antimiR-21 transfected MCF-7 cells and MDA-MB-231 cells.

2010-03-05 | GSE20627 | GEO

Homo sapiens

Project description:Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells

| PRJNA124819 | ENA

Antagonism of microRNA-122 in mice by systemically administered LNA-antimiR

Project description:Antagonism of microRNA-122 in mice by systemically administered LNA-antimiR leads to up-regulation of a large set of predicted target mRNAs in the liver MicroRNA-122 (miR-122) is an abundant liver-specific miRNA, implicated in fatty acid and cholesterol metabolism as well as hepatitis C viral replication. Here, we report that a systemically administered 16-nt, unconjugated LNA (locked nucleic acid)-antimiR oligonucleotide complementary to the 5' end of miR-122 leads to specific, dose-dependent silencing of miR-122 and shows no hepatotoxicity in mice. Antagonism of miR-122 is due to formation of stable heteroduplexes between the LNA-antimiR and miR-122 as detected by northern analysis. Fluorescence in situ hybridization demonstrated uptake of the LNA-antimiR in mouse liver cells, which was accompanied by markedly reduced hybridization signals for mature miR-122 in treated mice. Functional antagonism of miR-122 was inferred from a low cholesterol phenotype and de-repression within 24 h of 199 liver mRNAs showing significant enrichment for miR-122 seed matches in their 3' UTRs. Expression profiling extended to 3 weeks after the last LNA-antimiR dose revealed that most of the changes in liver gene expression were normalized to saline control levels coinciding with normalized miR-122 and plasma cholesterol levels. Combined, these data suggest that miRNA antagonists comprised of LNA are valuable tools for identifying miRNA targets in vivo and for studying the biological role of miRNAs and miRNA-associated gene-regulatory networks in a physiological context. Keywords: compound treatment

2008-12-16 | GSE13948 | GEO

Transcription profiling of mouse after antagonism of microRNA-122 by systemically administered LNA-antimiR

Project description:Antagonism of microRNA-122 in mice by systemically administered LNA-antimiR leads to up-regulation of a large set of predicted target mRNAs in the liver; MicroRNA-122 (miR-122) is an abundant liver-specific miRNA, implicated in fatty acid and cholesterol metabolism as well as hepatitis C viral replication. Here, we report that a systemically administered 16-nt, unconjugated LNA (locked nucleic acid)-antimiR oligonucleotide complementary to the 5' end of miR-122 leads to specific, dose-dependent silencing of miR-122 and shows no hepatotoxicity in mice. Antagonism of miR-122 is due to formation of stable heteroduplexes between the LNA-antimiR and miR-122 as detected by northern analysis. Fluorescence in situ hybridization demonstrated uptake of the LNA-antimiR in mouse liver cells, which was accompanied by markedly reduced hybridization signals for mature miR-122 in treated mice. Functional antagonism of miR-122 was inferred from a low cholesterol phenotype and de-repression within 24 h of 199 liver mRNAs showing significant enrichment for miR-122 seed matches in their 3' UTRs. Expression profiling extended to 3 weeks after the last LNA-antimiR dose revealed that most of the changes in liver gene expression were normalized to saline control levels coinciding with normalized miR-122 and plasma cholesterol levels. Combined, these data suggest that miRNA antagonists comprised of LNA are valuable tools for identifying miRNA targets in vivo and for studying the biological role of miRNAs and miRNA-associated gene-regulatory networks in a physiological context. Experiment Overall Design: Female NMRI mice were treated at day 2 with either 25mg/kg antimiR-122 (SPC3372) or vehicle (saline). Mice were sacrificied at day 3, 9 and 23 and liver RNA assayed. Three biological replicates for each of the six groups.

2009-01-13 | E-GEOD-13948 | biostudies-arrayexpress

GEP data from BCWM.1 cells treated with LNA antimiR-155 or scramble control

Project description:microRNA-155 acts as an oncogenic miRNA in B-cell lymphoproliferative disorders including Waldenstrom Macroglobulinemia (WM) and Chronic Lymphocytic Leukemia (CLL). we used an 8-mer LNA (locked nucleic acid) phosphorothioate oligonucleotide targeting the seed region of miR-155 to effectively antagonize in vitro tumor growth in WM. We performed gene expression profiling (GEP) analysis on BCWM.1 cells after treatment with LNA antimiR-155 or scramble control for 48 hours.

2012-07-09 | E-GEOD-39189 | biostudies-arrayexpress

Expression data from Lx-2 cells in which miR214 is repressed by LNA-antimiR-214

Project description:The expression of miR-214 is up-regulated in the liver of chronic viral hepatitis. Functional relevance of miR-214 was analyzed in human stellate cell line, Lx-2. Pro fibrotic genes were repressed, while translation related genes were up-regulated by LNA-antimiR-214

2018-04-01 | GSE57289 | GEO

MicroRNA155 mediates adverse inflammation in acute viral myocarditis LNA-antimiR155 treatment

Project description:For microRNA knockdown in vivo, a 15-mer LNA-antimiR oligonucleotide targeting mmu-miR-155 or an LNA control was administered to male 4-week-old C3H mice intravenously at a dose of 25 mg/kg per injection at days 1, 4 and 6 post-CVB3 infection. Samples were taken at 6 days post infection.

2012-06-06 | E-MEXP-3395 | biostudies-arrayexpress

Transcription profiling of human cells transfected with a miR-34a LNA inhibitor to investigate its role in oncogene-induced senescence

Project description:To understand the role of miR-34a in oncogene-induced senescence, we tested global mRNA expression using microarrays of TIG3 TERT/ deltaB-RAF:ER cells transfected with a miR-34a LNA inhibitor or a scrambled control LNA in the presence or absence of deltaB-RAF activation.<br>TIG3 TERT/ deltaB-RAF:ER cells are primary human diploid fibroblasts immortalized by hTERT. deltaB-RAF is constitutively active due to truncation of the regulatory N-terminal domain and fused to the hormone-binding domain of the oestrogen receptor, which was modified to respond to 4-hydroxytamoxifen (4-OHT) but not beta-estradiol.<br>TIG3 TERT/ deltaB-RAF:ER cells were treated with 500nM 4-OHT or equal amounts of ethanol the day after seeding at 1E6 per 10cm plate, in three biological replicates. After 2 days of 4-OHT treatment, cells were transfected with LNA-miR-34a or a control LNA-scramble using Lipofectamine 2000 (Invitrogen). Total RNA was harvested 24 h post-transfection (3 days of 4-OHT treatment in total) using TRIzol reagent. Affymetrix microarray analysis (HG-U133 Plus 2.0 human) was performed.

2009-08-01 | E-MEXP-2241 | biostudies-arrayexpress

YBX1-dependent LNA-tRF-mediated modulation of gene expression under hypoxia

Project description:In order to test whether inhibition of tRFs induced under hypoxia would counteract the YBX1-dependent reduction of target transcripts, we used transient transfection of antisense locked-nucleic acids (pooled LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr under hypoxia followed by microarray profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected (as a pool) in control and YBX1-knockdown cells under hypoxia to assess the consequences of inhibiting tRFs induced in hypoxic MDA-parental cells.

2015-05-08 | E-GEOD-63563 | biostudies-arrayexpress

Breast cancer MCF-7 Cells and MDA-MB-435 cells: pre-miR-125b Transfected cells vs. pre-control transfected cells

Project description:Transcriptional profiling of breast cancer cells comparing pre-control transfected cells with cells transfected with pre-miR-125b. We searched for miR-125b targets by systematic screening of mRNA profiling of pre-miR-125b transfected MCF-7 cells and MDA-MB-435 cells.

2010-06-25 | GSE22546 | GEO

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