Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1197734 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31704096_1.fastq.gz | Fastqsanger.gz | |||
| SRR31704096_2.fastq.gz | Fastqsanger.gz | |||
| SRR31704097_1.fastq.gz | Fastqsanger.gz | |||
| SRR31704097_2.fastq.gz | Fastqsanger.gz | |||
| SRR31704098_1.fastq.gz | Fastqsanger.gz |
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Project description:Smyd3 is a histone methyltransferase implicated in tumorigenesis. Here we show that Smyd3 expression in mice is required but not sufficient for chemically induced liver and colon cancer formation. In these organs Smyd3 is functioning in the nucleus as a direct transcriptional activator of several key genes involved in cell proliferation, epithelial-mesenchymal transition, JAK/Stat3 oncogenic pathways, as well as of the c-myc and b-catenin oncogenes. Smyd3 specifically interacts with H3K4Me3-modified histone tails and is recruited to the core promoter regions of many but not all active genes. Smyd3 binding density on target genes positively correlates with increased RNA Pol-II density and transcriptional outputs. The results suggest that Smyd3 is an essential transcriptional potentiator of a multitude of cancer-related genes. Standard Smyd3-deficient (Smyd3-KO) mice were generated using gene-trap ES cell clones (AS0527 from International Gene Trap Consortium), in which a selection cassette, containing the splice acceptor site from mouse EN2 exon 2 followed by the beta-galactosidase and neomycin resistance gene fusion gene and the SV40 polyadenylation sequence was inserted into the 5th intron of the Smyd3 gene. The resulting mice were devoid of Smyd3 mRNA and protein in all tissues, including liver and colon. For the generation of Smyd3-Tg mice the open reading frame of the mouse Smyd3 cDNA, which contained 3 Flag epitopes at the 3â end was inserted into the StuI site of the pTTR1-ExV3 plasmid (Yan et al, 1990). The 6.8 kb HindIII fragment containing the mouse transthyretin enhancer/promoter, intron 1, Smyd3 cDNA, three Flag epitopes and SV40 poly-A site was used to microinject C57Bl/6 fertilized oocytes. Founder animals were identified by Southern blotting and crossed with F1 mice to generate lines. Specific overexpression in the liver was tested by RT-PCR analysis in different tissues.
2016-07-03 | E-GEOD-67790 | biostudies-arrayexpress
Project description:To gain insight into how miR-142 deficit drives a BC-like transformation, we performed RNA-seq on bone marrow (BM) Lin-Sca-1+c-Kit+ cells (LSKs) harvested from normal miR-142+/+ (wt) and miR-142−/− (miR-142 KO) mice, as well as from leukemic miR-142+/+ BCR-ABL (CP CML) and miR-142−/− BCR-ABL (BC CML) mice, two weeks after BCR-ABL induction. We then performed gene expression profiling analysis using data obtained from RNA-seq of 24 samples of LSK cells from 4 mouse strains (KO vs WT, KO CML vs CML).
2022-11-01 | GSE216794 | GEO
Project description:We used CUT&RUN to evaluate the genome-wide mapping of human SMYD3 and H3K4me3 in HN-6 and 5-3 (SMYD3 KO) cells.
2024-11-01 | GSE280252 | GEO
Project description:We used RNA-seq to evaluate the transcriptomic changes induced by permanent SMYD3 KO in the HPV-negative head and neck squamous cell carcinoma cell lines HN-6.
2024-11-01 | GSE280251 | GEO
Project description:MiR-142 is dynamically expressed and plays a regulatory role in hematopoiesis. Based on the simple observation that miR-142 levels are significantly lower in CD34+CD38- cells from blast crisis (BC) chronic myeloid leukemia (CML). CML patients compared with chronic phase (CP) CML patients (p=0.002), we hypothesized that miR-142 deficit plays a role in BC transformation. To test this hypothesis, we generated a miR-142 KO BCR-ABL (i.e., miR-142−/−BCR-ABL) mouse by crossing a miR-142−/− mouse with a miR-142+/+BCR-ABL mouse. While the miR-142+/+BCR-ABL mice developed and died of CP CML, the miR-142−/−BCR-ABL mice developed a BC-like phenotype in the absence of any other acquired gene mutations and died significantly sooner than miR-142+/+BCR-ABL CP controls (p=0.001). Leukemic stem cell (LSC)-enriched Lineage-Sca-1+c-Kit+ cells (LSKs) from diseased miR-142−/−BCR-ABL mice transplanted into congenic recipients, recapitulated the BC features thereby suggesting stable transformation of CP-LSCs into BC-LSCs in the miR-142 KO CML mouse. Single cell (sc) RNA-seq profiling showed that miR-142 deficit changed the cellular landscape of the miR-142−/−BCR-ABL LSKs compared with miR-142+/+BCR-ABL LSKs with expansion of myeloid-primed and loss of lymphoid-primed factions. Bulk RNA-seq analyses along with unbiased metabolomic profiling and functional metabolic assays demonstrated enhanced fatty acid β-oxidation (FAO) and oxidative phosphorylation (OxPhos) in miR-142−/−BCR-ABL LSKs vs miR-142+/+BCR-ABL LSKs. MiR-142 deficit enhanced FAO in miR-142−/−BCR-ABL LSKs by increasing the expression of CPT1A and CPT1B, that controls the cytosol-to-mitochondrial acyl-carnitine transport, a critical step in FAO. MiR-142 deficit also enhanced OxPhos in miR-142−/−BCR-ABL LSKs by increasing mitochondrial fusion and activity. As the homeostasis and activity of LSCs depend on higher levels of these oxidative metabolism processes, we then postulate that miR-142 deficit is a potentially druggable target for BC-LSCs. To this end, we developed a novel CpG-miR-142 mimic oligonucleotide (ODN; i.e., CpG-M-miR-142) that corrected the miR-142 deficit and alone or in combination with a tyrosine kinase inhibitor (TKI) significantly reduced LSC burden and prolonged survival of miR-142−/−BCR-ABL mice. The results from murine models were validated in BC CD34+CD38- primary blasts and patient-derived xenografts (PDXs). In conclusion, an acquired miR-142 deficit sufficed in transforming CP-LSCs into BC-LSCs, via enhancement of bioenergetic oxidative metabolism in absence of any additional gene mutations, and likely represent a novel therapeutic target in BC CML.
2023-01-13 | ST002446 | MetabolomicsWorkbench
Project description:Purpose: The goal of this study was to compare the transcriptome of FACS-purified bone marrow BL/6 (WT) or CD93-/- (KO) LSKs and BL/6 (WT) or CD93-/- (KO) LSCs. We also compared the transcriptome of FACS-purified bone marrow LSCs isolated from BL/6 mice previously treated with MCP or Veh in vivo. Methods: Transcriptomic analysis of CD93-proficient and deficient bone marrow LSKs and CML LSCs or CML LSCs upon treatment with MCP or Veh, were assessed in biological replicates using Illumina. qRT–PCR validation was performed using SYBR Green assays. Results: We mapped around 30 million sequence reads per sample to the mouse genome (GRCm38 - mm10) and identified expressed transcripts in studied samples. RNA-seq data confirmed stable expression of known housekeeping genes. Differentially expressed genes among conditions were identified with a fold change ≥1.5 and FDR p-value <0.05. Conclusions: Our study represents the first detailed transcriptome analysis of CD93-proficient and deficient bone marrow LSKs and LSCs isolated from BM of naïve and CML mice generated by RNA-seq. technology. Our results show that CD93-signaling triggers stem cell maintenance- and cell proliferation-promoting signaling pathways in CML LSCs. In addition, we showed transcriptome analysis of FACS-purified bone marrow LSCs isolated from BL/6 (WT) mice which were previously treated with MCP or Veh in vivo. Our results show that MCP treatment suppresses the stem cell maintenance- and cell proliferation-promoting signaling pathways in CML LSCs.
2021-02-07 | GSE149358 | GEO
Project description:RNA-sequencing analysis of control and SMYD3-knockdown MDA-MB-231 tumors from the mammary glands of orthotopic xenograft NOD/SCID mice. SMYD3 (also known as KMT3E), a hisone H3 lysine K4 methyltransferase, is highly expressed in several human cancers, including colorectal and breast carcinomas. Results provide insight into the transcriptional regulation of SMYD3 in breast cancer.
2020-06-30 | GSE129268 | GEO
Project description:Members of the SMYD family of Histone Lysine Methyltransferases, including SMYD3, were shown to be involved in both cardiac and skeletal myogenesis. Currently, very little is known about their mechanisms of action and their potential target genes. To study the cellular and molecular function of SMYD3 in skeletal muscle differentiation, we used loss and gain of function approaches in C2C12 myoblasts. We used RNA sequencing (RNA-seq) to generate gene expression profiling during myogenic differentiation under SMYD3 transient knockdown by siRNAs or SMYD3 stable overexpression in C2C12. We identified multiple genes whose expression is significantly affected by Smyd3 levels, among them the key myogenic regulatory factor (MRF) Myogenin.
2019-09-25 | GSE137954 | GEO
Project description:Purpose: The goal of this study was to compare transcriptome profile of FACS-purified bone marrow (BM) Tregs isolated from CML or naive mice. Methods: Transcriptomic profiles of BM Tregs from CML or naïve mice were assessed in biological replicates using Illumina NextSeq 500. Results: We mapped around 30 million sequence reads per sample to the mouse genome (GRCm38 - mm10) and identified expressed transcripts in FACS-purified BM Tregs isolated from CML or naive mice. RNA-seq data confirmed stable expression of known housekeeping genes. Differentially expressed genes between Tregs derived from the BM of CML and naïve mice were identified. Conclusions: Our study represents the first detailed RNA-seq analysis of FACS-purified BM Tregs isolated from CML or naive mice. Our results show that Tregs derived from the BM of CML mice have an increased metabolic activity, cell cycle activity and immunosuppressive capacity.
2021-11-03 | GSE174190 | GEO