Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE20627 | GEO | 2010/03/05
SECONDARY ACCESSION(S): PRJNA124819
REPOSITORIES: GEO
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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. Two-condition experiment, LNA-antimiR-21 Transfected vs. LNA-control Transfected MCF-7 cells. One replicate per array.
2010-05-06 | E-GEOD-20627 | biostudies-arrayexpress
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2008-12-16 | GSE13948 | GEO
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
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.
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Project description:Investigation of whole genome gene expression level changes in African Green Monkeys treated with antimiR-33a/b, compared to the animal treated with vehicle The treatment of the monkeys is further described in Rottiers V, Obad S, McGarrah R, Black JC, Lindholm M, Goody R, Lawrence M, Whetstine JR, Gerszten RE, Kauppinen S, Näär AM. (2013). Pharmacological inhibition of a microRNA family in non-human primates by a seed-targeting 8-mer antimiR oligonucleotide. Accepted for publication at Science Translational Medicine. MicroRNAs (miRNAs) regulate many aspects of human biology. They target mRNAs for translational repression or degradation through base-pairing with 3’ UTRs, primarily via seed sequences (nucleotides 2-8 in the mature miRNA sequence). A number of individual miRNAs and miRNA families share seed sequences and targets, but differ in the sequences outside of the seed. miRNAs have been implicated in the etiology of a wide variety of human diseases and therefore represent promising therapeutic targets. However, potential redundancy and compensatory action of different miRNAs sharing the same seed sequence, and the challenge of simultaneously targeting miRNAs that differ significantly in non-seed sequences complicates therapeutic targeting approaches. We recently demonstrated effective inhibition of entire miRNA families using seed-targeting 8-mer locked nucleic acid (LNA)-modified antimiRs in short-term experiments in mammalian cells and in mice. However, the long-term efficacy and safety of this approach in higher organisms, such as humans and non-human primates, has not been determined. Here, we show that pharmacological inhibition of the miR-33 family, key regulators of cholesterol/lipid homeostasis, by a subcutaneously delivered 8-mer LNA-modified antimiR in obese and insulin-resistant non-human primates results in de-repression of miR-33 targets, such as ABCA1, increases circulating high-density lipoprotein-cholesterol (HDL-C), and is well tolerated over 108 days of treatment. These findings demonstrate the efficacy and safety of an 8-mer LNA-antimiR against a miRNA family in a non-human primate metabolic disease model, suggesting that this could be a feasible approach for therapeutic targeting of miRNA families sharing the same seed sequence in human diseases.
2013-08-23 | GSE50116 | GEO
Project description:Investigation of whole genome gene expression level changes in African Green Monkeys treated with antimiR-33a/b, compared to the animal treated with vehicle The treatment of the monkeys is further described in Rottiers V, Obad S, McGarrah R, Black JC, Lindholm M, Goody R, Lawrence M, Whetstine JR, Gerszten RE, Kauppinen S, NM-CM-$M-CM-$r AM. (2013). Pharmacological inhibition of a microRNA family in non-human primates by a seed-targeting 8-mer antimiR oligonucleotide. Accepted for publication at Science Translational Medicine. MicroRNAs (miRNAs) regulate many aspects of human biology. They target mRNAs for translational repression or degradation through base-pairing with 3M-bM-^@M-^Y UTRs, primarily via seed sequences (nucleotides 2-8 in the mature miRNA sequence). A number of individual miRNAs and miRNA families share seed sequences and targets, but differ in the sequences outside of the seed. miRNAs have been implicated in the etiology of a wide variety of human diseases and therefore represent promising therapeutic targets. However, potential redundancy and compensatory action of different miRNAs sharing the same seed sequence, and the challenge of simultaneously targeting miRNAs that differ significantly in non-seed sequences complicates therapeutic targeting approaches. We recently demonstrated effective inhibition of entire miRNA families using seed-targeting 8-mer locked nucleic acid (LNA)-modified antimiRs in short-term experiments in mammalian cells and in mice. However, the long-term efficacy and safety of this approach in higher organisms, such as humans and non-human primates, has not been determined. Here, we show that pharmacological inhibition of the miR-33 family, key regulators of cholesterol/lipid homeostasis, by a subcutaneously delivered 8-mer LNA-modified antimiR in obese and insulin-resistant non-human primates results in de-repression of miR-33 targets, such as ABCA1, increases circulating high-density lipoprotein-cholesterol (HDL-C), and is well tolerated over 108 days of treatment. These findings demonstrate the efficacy and safety of an 8-mer LNA-antimiR against a miRNA family in a non-human primate metabolic disease model, suggesting that this could be a feasible approach for therapeutic targeting of miRNA families sharing the same seed sequence in human diseases. Expression analysis study in obese Non Human Primates (African Green Monkeys). Five animals treated with antimiR-33a/b were compared to five animals treated with vehicle.
2013-08-23 | E-GEOD-50116 | biostudies-arrayexpress
Project description:Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells
| PRJNA124819 | ENA
Project description:HeLa cells transfected with LNA-antimiR's against miR-21.
2011-07-05 | E-MEXP-2803 | biostudies-arrayexpress