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Expression analysis of mice hepatic NMuLi cells treated LNA gapmer ASO containing nucleobase modification

ABSTRACT: Expression analysis of mice hepatic NMuLi cells treated LNA gapmer ASO containing nucleobase modification

PROVIDER: PRJNA809303 | ENA |

REPOSITORIES: ENA

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Expression analysis of mice hepatic NMuLi cells treated LNA gapmer ASO containing nucleobase modification

Project description:Antisense oligonucleotide (ASO) has the potential to induce hybridization-dependent effects by inadvertent binding of ASOs to RNA with sequences similar to that of the target RNA. In the present study, we examined the effects of the nucleobase derivatives introduced into the gapmer ASOs on gene expression. We performed microarray analysis using NMuLi cells (mouse liver-derived cells) treated with LNA gapmer ASO containing nucleobase modification.

2022-07-12 | GSE197166 | GEO

Expression analysis of Huh-7 cells treated with LNA gapmer targeting glucocorticoid receptor (GR) RNA

Project description:Antisense oligonucleotide (ASO) has the potential to induce off-target effects due by inadvertent binding of ASOs to unintended RNAs that have a sequence similar to the target RNA. In the present study, we focused on the effects of oligonucleotide extension of gapmer ASOs on off-target effects. We performed microarray analysis using Huh-7 cells (human liver-derived cells) treated with a 14-mer LNA gapmer ASO and the extended 18-mer derivatives with the same core 14-mer region.

2021-12-15 | GSE188684 | GEO

Evaluation of off-target effects of gapmer antisense oligonucleotides using human cells

Project description:Antisense oligonucleotide (ASO) has the potential to induce off-target effects due to complementary binding between the ASO and unintended RNA with a sequence similar to the target RNA. In this study, we evaluated off-target effects of gapmer ASOs, which cleave the target RNA in an RNase H-dependent manner, by introducing the ASO into human cells and performing microarray analysis. Our data indicate that gapmer ASOs induce off-target effects depending on the degree of complementarity between the ASO and off-target candidate genes. Based on our results, we also propose a scheme for assessment of off-target effects of gapmer ASOs.

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Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity

Project description:Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity

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Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity

Project description:The biological role and therapeutic potential of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) are still to be investigated. Here, we studied the functional significance and the druggability of the oncogenic lncRNA MALAT1 in MM. Targeting MALAT1 by novel LNA-gapmeR anti-sense oligonucleotide antagonized MM cell proliferation and triggered apoptosis both in vitro and in vivo in a murine xenograft model of human MM. Of note, antagonism of MALAT1 dowmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1-targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.

2018-12-31 | GSE108824 | GEO

Antisense oligonucleotides modified with a boron cluster and a cholesterol moiety (B-ASO-LNA-CHOL)

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Gene expression profile of modified gapmer antisense oligonucleotides treated mouse liver

Project description:To investigate gene expression change induced by modified gapmer antisense oligonucleotides, we performed transcriptome analysis of Scarb1 ASO or PBS treated mouse livers.

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Expression analysis of Huh-7 cells treated with LNA gapmer targeting glucocorticoid receptor (GR) RNA

Project description:Expression analysis of Huh-7 cells treated with LNA gapmer targeting glucocorticoid receptor (GR) RNA

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Knockdown of circular RNAs using LNA-modified antisense oligonucleotides

Project description:Circular RNAs (circRNAs) constitute an abundant class of covalently closed non-coding RNA molecules that are formed by backsplicing from eukaryotic protein-coding genes. Recent studies have shown that circRNAs can act as microRNA or protein decoys as well as transcriptional regulators. However, the functions of most circRNAs are still poorly understood. Because circRNA sequences overlap with their linear parent transcripts, depleting specific circRNAs without affecting host gene expression remains a challenge. Here, we assessed the utility of LNA-modified antisense oligonucleotides (ASOs) to knock down circRNAs for loss-of-function studies. We identified 5807 circRNAs in total RNA sequencing data from 4 liver cancer cell lines and used the back splice junction (BSJ) sequences of 7 validated circRNAs as target sites for designing different LNA-modified ASOs for circRNA knockdown. We found that while most RNase H-dependent gapmer ASOs mediate effective knockdown of their target circRNAs, some gapmers reduce the levels of the linear parent transcript and may also cause degradation of unintended off-targets. The circRNA targeting specificity can be enhanced using design-optimized gapmer ASOs or LNA/DNA mixmer ASOs, which display potent and specific circRNA knockdown with a minimal effect on the host genes or predicted off-targets. In summary, our results demonstrate that LNA-modified ASOs complementary to BSJ sequences mediate robust knockdown of circRNAs in vitro and, thus, represent a useful tool to explore the biological roles of circRNAs in loss-of-function studies in cultured cells and animal models.

2022-11-01 | GSE145592 | GEO

Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity.

Project description:The biological role and therapeutic potential of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) are still to be investigated. Here, we studied the functional significance and the druggability of the oncogenic lncRNA MALAT1 in MM. Targeting MALAT1 by novel LNA-gapmeR antisense oligonucleotide antagonized MM cell proliferation and triggered apoptosis both in vitro and in vivo in a murine xenograft model of human MM. Of note, antagonism of MALAT1 downmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1 targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.

| S-EPMC6127082 | biostudies-literature

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