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Loss of function of MALAT1 on primary human OA osteoblast transcriptome

ABSTRACT: Cells: Primary human osteoblasts from subchondral bone of osteoarthritis patients (n=3 patients). Treatments: Cells transfected using Lipofectamine 3000 (Qiagen) with either control LNA (NC) or MALAT1 LNA1 or MALAT1 LNA2 for 24 hours. Total RNA extracted by Qiagen RNeasy columns. RIN values >7 via Agilent Bioanalyser. Analysis: RNA subjected to Quantseq 3' RNA sequencing (Lexogen) and sequenced reads mapped to the hg38 reference human genome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE167918 | GEO | 2021/04/28

REPOSITORIES: GEO

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Differential Gene expression in the mouse mammary tumors of PyMT-Malat1 wild-type (WT), PyMT-Malat1 knockout (KO) and PyMT-Malat1 knockout with Malat1 transgene expression (TG)

Project description:Previously, lncRNA Malat1 knockout mice were generated by insertional inactivation. By crossing this line to MMTV-PyMT mammary tumor mouse model, we produced PyMT;Malat1 wild-type (WT) and PyMT;Malat1 knockout (KO). Furthermore, we generated Malat1 transgenic mice by targeting ROSA26 locus and bred them to PyMT;Malat1 knockout mice to produce Malat1-rescued PyMT;Malat1 knockout;Malat1 transgenic animals (TG). Using mammary tumors from the three groups of animals, we performed RNA-Seq analysis to identify differentially up-regulated genes in KO tumors to find novel target genes of YAP-TEAD pathway.

2018-09-18 | GSE110239 | GEO

Effects of the long noncoding RNA Malat1 on gene expression [Mouse430_2]

Project description:Malat1 is an abundant long noncoding RNA that localizes to nuclear bodies known as nuclear speckles, which contain a distinct set of pre-mRNA processing factors. Previous in vitro studies have demonstrated that Malat1 interacts with pre-mRNA splicing factors, including the serine- and arginine-rich (SR) family of proteins, and regulates a variety of biological processes, including cancer cell migration, synapse formation, cell cycle progression, and responses to serum stimulation. To address the physiological function of Malat1 in a living organism, we generated Malat1-KO (KO) mice using homologous recombination. Unexpectedly, the Malat1-KO mice were viable and fertile, showing no apparent phenotypes. Nuclear speckle markers were also correctly localized in cells that lacked Malat1. However, the cellular levels of another long noncoding RNA, Neat1, which is an architectural component of nuclear bodies known as paraspeckles, were downregulated in a particular set of tissues and cells lacking Malat1. To address if the the absence of Malat1 affects the expression of other genes, including other long noncoding RNA, microarrays were used to study the impact of knocking-out Malat1 on global gene expression in mouse embryonic fibroblasts (MEFs). MEFs were prepared from E13.5 mouse embryos from wildtype and Malat1 knock-out mice. RNA harvested from these cells were hybridized to Affymetirx mouse gene expression array.

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2018-10-26 | PXD005154 | Pride

Transcriptome 3' end profiling by high throughput sequencing of HeLa cells depleted of MATR3, PTBP1/2 individually or in combination.

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Effects of the long noncoding RNA Malat1 on gene expression

Project description:This SuperSeries is composed of the following subset Series: GSE37705: Effects of the long noncoding RNA Malat1 on gene expression [Mouse430_2] GSE37706: Effects of the long noncoding RNA Malat1 on gene expression [MoEx-1_0-st] Refer to individual Series

2012-06-24 | E-GEOD-37707 | biostudies-arrayexpress

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

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Project description:The main aim was to determine how polyadenylation site usage is affected by osteoarthritis. Age matched tissue samples were obtained from both healthy individuals and those with late stage osteoarthritis, total RNA was isolated and then QuantSeq Reverse library produced using commercial kit (Lexogen) before sequencing

2022-10-01 | E-MTAB-12184 | biostudies-arrayexpress

Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB

Project description:The long noncoding MALAT1 RNA is upregulated in cancer tissues and its elevated expression is associated with hyper-proliferation, but the underlying mechanism is poorly understood. We demonstrate that MALAT1 levels are regulated during normal cell cycle progression. Genome-wide transcriptome analyses in normal human diploid fibroblasts reveal that MALAT1 modulates the expression of cell cycle genes, and is required for G1/S and mitotic progression. Depletion of MALAT1 leads to activation of p53 and its target genes. The cell cycle defects observed in MALAT1-depleted cells are sensitive to p53 levels, indicating that p53 is a major downstream mediator of MALAT1 activity. Furthermore, MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing. In human cells, MALAT1 promotes cellular proliferation by modulating the expression and/or premRNA processing of cell cycle-regulated transcription factors. These findings provide mechanistic insights on the role of MALAT1 in regulating cellular proliferation. Keywords: MALAT1; MALAT-1, NEAT2, ncRNA; E2F, alternative splicing; pre-mRNA splicing factors WI38 cells (normal human diploid fibroblasts) were transfected with a control oligo (CTR) or antisense oligos to MALAT1 and RNA was isolated after 48 hr. Two antisense oligos were use for MALAT1 (AS-1 and AS-2). Arrays were done for 3 sets of samples in triplicate (control, AS-1 and AS-2).

2014-05-16 | E-GEOD-44240 | biostudies-arrayexpress

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