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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)

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE110239 | GEO | 2018/09/18

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: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)

| PRJNA433234 | 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

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

2016-01-12 | GSE67647 | GEO

Next generation sequencing of neutrophils from WT, PyMT and PyMT-Cxcr2-/- mice

Project description:We report the comparison of gene expression of neutrophils in the mammary gland of PyMT and PyMT-Cxcr2-/- animals as well as the one of WT bone marrow

2021-05-21 | GSE164766 | GEO

Whole genome transcriptional profile of PyMT/SIRT6 vs PyMT mammary tumors

Project description:We compared the transcriptional profile of mammary tumors spontaneously developed in PyMT transgenic mice either bearing or not additional copies of the endogeneous SIRT6 gene.

2017-01-20 | GSE93837 | GEO

Effects of the long noncoding RNA Malat1 on gene expression [MoEx-1_0-st]

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 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 hippocampal neurons. Hippocampi were dissected from two sets of wildtype and Malat1 knock-out mice and RNA from these neurons were hybridized to Affymetix mouse exon array. Individual animals from each pairs of wildtype and knock-out are littermates.

2012-06-24 | E-GEOD-37706 | biostudies-arrayexpress

Transcription profiling of mouse AKR/J x PyMT F1 versus DBA/2J x PyMT F1 tumors

Project description:F1 hybrids from (AKR/J x FVB/NJ) and (DBA/2J x FVB/NJ) outcrosses display a 20-fold difference in mammary tumor metastatic capacity, due to differences in inherited polymorphisms. Expression studies were performed to determine whether polymorphism-driven gene expression signatures predictive of outcome could be generated from mouse tumor tissues Experiment Overall Design: Mammary tumors from adult F1 animals from (AKR/J x PyMT) and (DBA/2J x PyMT) outcrosses was collected and arrayed on Affymetrics chip to identify basal differences in gene expression between the different genotypes

2009-01-13 | E-GEOD-13221 | biostudies-arrayexpress

Genome-wide maps in mammary glands of MMTV-PyMT mice with or without miR-9 knockout.

Project description:Analysis of the transcriptome change of mammary glands of MMTV-PyMT mice with or without miR-9 knockout. MiR-9 regulates various transcripts and signaling pathways.Results provide insight into the role of miR-9-involved mechanisms underlying miR-9-mediated effects on breast cancer progression.

2024-03-01 | GSE202307 | GEO

Consequences of sEH deletion in the polyoma middle T (PyMT) breast cancer tumor proteome

Project description:The aim of this investigation was to study the consequences of interfering with soluble epoxide hydrolase (sEH) expression on tumor growth and metastasis in genetically modified animals that spontaneously generate tumors without the exogenous application of high concentrations of epoxide mediators or inhibitors. Therefore, breast cancer development was studied in mice expressing the polyoma middle T oncogene (PyMT) under the control of the mouse mammary tumor virus promoter, to induce spontaneous mammary tumors. To facilitate the study of endogenous sEH activity in tumor growth, PyMT mice were then crossed with sEH-/- mice to generate sEH-deficient mice that spontaneously generate breast tumors (so called PyMTsEH mice). For these analyses, primary tumors were removed from 20 week old mice.

2021-09-14 | PXD026214 | Pride

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.

2012-06-24 | E-GEOD-37705 | biostudies-arrayexpress

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