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Effect of lncRNA MALAT1 knockdown on miRNA expression of EC109 cells

ABSTRACT: Effect of lncRNA MALAT1 knockdown on miRNA expression of EC109 cells

PROVIDER: PRJNA863288 | ENA |

REPOSITORIES: ENA

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Effect of lncRNA MALAT1 knockdown on miRNA expression of EC109 cells

Project description:Microarrays were used to characterize the global changes in miRNA expression in EC109 cells due to siRNA knockdown of long non-coding RNA MALAT1

2024-01-23 | GSE209995 | GEO

Effect of lncRNA MALAT1 knockdown on gene expression of EC109 cells

Project description:microarrays were used to characterize the global changes in gene expression in EC109 cells due to siRNA knockdown of long non-coding RNA MALAT1

2024-01-23 | GSE209963 | GEO

Effect of lncRNA MALAT1 knockdown on gene expression of EC109 cells

Project description:Effect of lncRNA MALAT1 knockdown on gene expression of EC109 cells

| PRJNA863241 | ENA

Differentiation of Mammary Tumors and Reduction in Metastasis Upon Malat1 LncRNA Loss

Project description:Genome-wide analyses have identified thousands of long non-coding RNAs (lncRNAs). Malat1 (Metastasis Associated Lung Adenocarcinoma Transcript 1) is among the most abundant lncRNAs whose expression is altered in numerous cancers. Here we report that genomic loss, as well as systemic knockdown of Malat1 using antisense oligonucleotides, in the MMTV-PyMT mouse mammary carcinoma model results in slower tumor growth accompanied by differentiation into highly cystic tumors and a significant reduction in lung metastasis. Further, Malat1 loss results in a reduction of branching morphogenesis in MMTV-PyMT and Her2/neu amplified tumor organoids consistent with the in vivo reduction in lung metastasis. At the molecular level, Malat1 knockdown results in alterations in gene expression and changes in splicing patterns of genes involved in differentiation and pro-tumorigenic signaling pathways. Together, these data indicate that the lncRNA Malat1 regulates critical processes in mammary cancer pathogenesis and represents a promising therapeutic target for inhibiting breast cancer metastasis. Transcriptome profiles of tumors and organoids after Malat1 knockdown using antisense olgonucleotides (ASOs).

2016-01-12 | E-GEOD-67647 | biostudies-arrayexpress

Alternative splicing modulation mediated by G-quadruplex structures in MALAT1 lncRNA

Project description:MALAT1, an abundant lncRNA specifically localized to nuclear speckles, regulates alternative-splicing (AS). The molecular basis of its role in AS remains poorly understood. Here, we report three conserved, thermodynamically stable, parallel RNA-G-quadruplexes (rG4s) present in the 3’ region of MALAT1 which regulates this function. Using rG4 domain specific RNA-pull-down followed by mass-spectrometry, RNA-immuno-precipitation and imaging, we demonstrate the rG4 dependent localization of Nucleolin (NCL) and Nucleophosmin (NPM) to nuclear speckles. Specific G-to-A mutations that abolish rG4 structures, results in the localization loss of both the proteins from speckles. Functionally, disruption of rG4 in MALAT1 phenocopies NCL knockdown resulting in altered pre-mRNA splicing of endogenous genes. These results reveal a central role of rG4s within the 3’ region of MALAT1 orchestrating AS.

2022-02-17 | PXD026386 | Pride

lncRNA MALAT1 interactome - Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation

Project description:Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA) that was first discovered as a prognostic marker for lung cancer metastasis. MALAT1 has been implicated in the tumorigenesis of numerous tumor types. To further delineate the underlying molecular mechanism, we established a high-throughput strategy to characterize the interacting proteins of MALAT1 by combining RNA pull down, quantitative proteomics, bioinformatics analysis, and experimental validation.

2018-10-26 | PXD005154 | Pride

High-throughput sequencing identified differentially expressed RNAs between MALAT1 knockdown C3H10 adipocyte and control cells

Project description:Although MALAT1 is a lncRNA highly expressed in many tissues and participates in a series of physiological and pathological processes, the potential role of MALAT1 in adipogenesis is not clear. To gain full insights into MALAT1 function in the adipogenic differention of C3H10 cell, we performed RNA-seq to antisense oligonucleotides(ASO) treated C3H10 cells and found numerous differentially expressed RNAs between MALAT1 knockdown C3H10 adipocyte and control cells.

2020-09-07 | GSE156615 | GEO

Differentiation of Mammary Tumors and Reduction in Metastasis Upon Malat1 LncRNA Loss

2016-01-12 | GSE67647 | GEO

Gene expression profiling of mouse macrophages following long noncoding RNA Malat1 knockdown

Project description:We applied next-generation sequencing to investigate the gene expression profiles in mouse bone-marrow derived macrophages with or without long noncoding RNA-Malat1 knockdown. We identified a number of differentially regulated genes in cells with Malat1 knockdown.

2017-11-18 | GSE106913 | GEO

The key regulation of LncRNA MALAT1/miR-124-3p/PI3K axis during reprogramming of primary mouse hepatocytes into insulin-producing cells

Project description:In this study, a considerable augmentation in the expression of the endogenous long noncoding RNA MALAT1 (lncRNA MALAT1) and PI3K was discerned, in contrast to a significant diminution in miR-124-3p expression, during the progression of in vitro induced differentiation of primary mouse hepatocytes. Bioinformatics scrutiny and the luciferase reporter assay unveiled the binding of miR-124-3p to specific loci in lncRNA MALAT1 and PI3K, suppressing their expression. Elevated expression of lncRNA MALAT1 potently diminished the expression levels of PI3K and attenuated the efficacy of primary mouse hepatocytes differentiation into insulin-producing cells. Furthermore, the in vitro responsiveness of primary mouse hepatocytes-derived β islet-like cells to high glucose stimuli and insulin release by these cells were significantly diminished in the overexpression of lncRNA MALAT1 transfection group, while the outcomes were converse in the si-lncRNA MALAT1 group. The experimental findings suggest that lncRNA MALAT1 effectively sustains PI3K gene expression through competitive binding to miR-124-3p, accomplishing regulation of primary mouse hepatocytes directed β islet-like cell differentiation efficiency.

2025-07-16 | GSE269392 | GEO

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