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ABSTRACT: RNA sequencing of Men1-WT and Men1-KO mouse lung tissues

PROVIDER: PRJNA888804 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21848955_1.fastq.gz	Fastqsanger.gz
	SRR21848955_2.fastq.gz	Fastqsanger.gz
	SRR21848956_1.fastq.gz	Fastqsanger.gz
	SRR21848956_2.fastq.gz	Fastqsanger.gz
	SRR21848957_1.fastq.gz	Fastqsanger.gz

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The function of Men1 and kmt2a gene in lung of mice

Project description:To explore the target genes of Men1 and Kmt2a in lung of mice, we isolated the lung tissues from WT and Men1 knockout and Kmt2a mouse and performed gene expression profiling analysis by RNA-seq.

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Loss of MEN1 activates DNMT1 implicating DNA hypermethylation as a driver of MEN1 tumorigenesis

Project description:Multiple endocrine neoplasia type 1 (MEN1) syndrome is the result of mutations in the MEN1 gene and results in tumor formation via mechanisms that are not well understood. Using a novel genome-wide methylation analysis, we studied tissues from patients with MEN1-parathyroid tumors, tissues from Men1 knockout (KO) mouse models, and mouse Men1 null mouse embryonic fibroblast (MEF) cell lines. Tissues from KO mice were used to confirm and assess the findings from the MEN1 clinical samples and further explore the molecular mechanisms of global epigenetic changes following the inactivation of menin. We demonstrated that the inactivation of menin results in enhanced activity of DNA (cytosine-5)-methyltransferase 1 (DNMT1) by retinoblastoma-binding protein 5 (Rbbp5) activation in MEN1 tumor tissues. The increased activity of DNMT1 mediated global DNA hypermethylation, which in turn resulted in aberrant activation of the Wnt/Î²-catenin signaling pathway through inactivation of Sox regulatory genes. Our study provides important insights into the possible regulatory role of menin in DNA methylation and its impact on the pathogenesis of MEN1 tumor development. Global DNA methylation in tissues from patients with MEN1-parathyroid tumors. Thirty-eight human parathyroid specimens were used: 13 sporadic (non-MEN1) parathyroid adenomas, 12 MEN1-parathyroid tumors, 4 parathyroid carcinomas, and 9 normal parathyroids.

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Project description:RNA sequencing of MEN1-WT and MEN1-KO NCI-H460 cells

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Differentially regulated genes in adipocytes derived from Men1-null vs WT mouse embryonic stem cells

Project description:MEN1 is a tumor suppressor gene loss of which causes lipoma (fatty tumors under the skin) and many other endocrine and non-endocrine tumors. It's target genes in fat cells (adipocytes) are unknown. Gene expression in adipocytes that were in vitro differentiated from mouse embryonic stem cells (mESCs) of Men1-nul l(Men1-KO) and WT mice were compared to assess the expression of genes upon menin loss in adipocytes that could lead to the deveopment of lipoma. mESCs (Men1-null and WT) were in vitro differentaited into adipocytes. Positive oil red O staining indicated successful differentiation into adipocytes. The cells were processed for RNA isolation. RNA preps were used for microarray analysis.

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Loss of MEN1 activates DNMT1 implicating DNA hypermethylation as a driver of MEN1 tumorigenesis

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Project description:RNA-Seq of Men1-KO mouse hippocampus

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Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (ChIP-Seq)

Project description:Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. To study the role of menin-dependent H3K4me3, we performed in vitro differentiation of wild-type as well as menin-null mouse embryonic stem cells (mESCs) into pancreatic islet-like endocrine cells (PILECs). Gene expression analysis and genome-wide H3K4me3 ChIP-Seq profiling in wild-type and menin-null mESCs and PILECs revealed menin-dependent H3K4me3 at the imprinted Dlk1-Meg3 locus in mESCs, and all four Hox loci in differentiated PILECs. Specific and significant loss of H3K4me3 and gene expression was observed for genes within the imprinted Dlk1-Meg3 locus in menin-null mESCs and the Hox loci in menin-null PILECs. Given that the reduced expression of genes within the DLK1-MEG3 locus and the HOX loci is associated with MEN1-like sporadic tumors, our data suggests a possible role for menin-dependent H3K4me3 at these genes in the initiation and progression of sporadic pancreatic endocrine tumors. Furthermore, our investigation also demonstrates that menin-null mESCs can be differentiated in vitro into islet-like endocrine cells, underscoring the utility of menin-null mESC-derived specialized cell types for genome-wide high-throughput studies. Genome-wide mapping of H3K4me3 and microarray gene expression profiling in TC-1 wild-type (WT) mESCs, menin-null (Men1-ko) mESCs (3.2N), pancreatic islet-like endocrine cells (PILECs) derived from WT mESCs, and PILECs derived from Men1-ko mESCs.

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Gene expression profiling of WT and Aldh1a1 KO mouse lung tissues

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