RNA sequencing of Sphk1fl/fl Sphk2-/- and Sphk1-/- Sphk2-/- mESC clones.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA587753 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10402100_1.fastq.gz | Fastqsanger.gz | |||
| SRR10402100_2.fastq.gz | Fastqsanger.gz | |||
| SRR10402101_1.fastq.gz | Fastqsanger.gz | |||
| SRR10402101_2.fastq.gz | Fastqsanger.gz | |||
| SRR10402090_1.fastq.gz | Fastqsanger.gz |
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Project description:The study analyzes analyzes gene expression changes in the ankle joint in mouse TNFa overexpression models with or without sphingosine kinase 1 activity. SphK1 is a sphingolipid enzyme that converts sphingosine to bioactive sphingosine-1-phosphate (S1P). Recent data suggest a potential relationship between SphK1 and TNFα and have implicated SphK1/S1P in the development and progression of inflammation. Here we further study the relationship of TNFα and SphK1 using an in vivo model. Transgenic hTNFα mice, which develop a spontaneous arthritis (limited to paws) at 20 weeks, were crossed with SphK1 activity null mice (SphK1-/-) to study the development of inflammatory arthritis in the functional absence of SphK1. Results show that hTNF/SphK1-/- have significantly less severity and progression of arthritis and bone erosions as measured through micro-CT images. Additionally, less COX-2 protein, mTNFα transcript levels and fewer Th 17 cells were detected in the joints of hTNF/SphK1-/- compared to hTNF/SphK1+/+ mice. Microarray analysis of the ankle joint showed that hTNF/SphK1-/- mice have increased transcript levels of IL-6 and SOCS3 compared to hTNF/SphK1+/+ mice. Finally, fewer mature osteoclasts were detected in the ankle joints of hTNF/SphK1-/- mice compared to hTNF/SphK1+/+ mice. These data show that SphK1 plays a role in hTNFα induced inflammatory arthritis, potentially through a novel pathway involving IL-6 and SOCS3. Two wild-type replicates; three replicates of human TNFa transgene overexpression and normal sphingosine kinase 1; three replicates of human TNFa transgene overexpression and sphingosine kinase 1 null.
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Project description:The study analyzes analyzes gene expression changes in the ankle joint in mouse TNFa overexpression models with or without sphingosine kinase 1 activity. SphK1 is a sphingolipid enzyme that converts sphingosine to bioactive sphingosine-1-phosphate (S1P). Recent data suggest a potential relationship between SphK1 and TNFα and have implicated SphK1/S1P in the development and progression of inflammation. Here we further study the relationship of TNFα and SphK1 using an in vivo model. Transgenic hTNFα mice, which develop a spontaneous arthritis (limited to paws) at 20 weeks, were crossed with SphK1 activity null mice (SphK1-/-) to study the development of inflammatory arthritis in the functional absence of SphK1. Results show that hTNF/SphK1-/- have significantly less severity and progression of arthritis and bone erosions as measured through micro-CT images. Additionally, less COX-2 protein, mTNFα transcript levels and fewer Th 17 cells were detected in the joints of hTNF/SphK1-/- compared to hTNF/SphK1+/+ mice. Microarray analysis of the ankle joint showed that hTNF/SphK1-/- mice have increased transcript levels of IL-6 and SOCS3 compared to hTNF/SphK1+/+ mice. Finally, fewer mature osteoclasts were detected in the ankle joints of hTNF/SphK1-/- mice compared to hTNF/SphK1+/+ mice. These data show that SphK1 plays a role in hTNFα induced inflammatory arthritis, potentially through a novel pathway involving IL-6 and SOCS3.
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Project description:The oncogenic roles of Sphingosine kinase 1 (SphK1) in various cancers, including thyroid cancer, have been well demonstrated. However, miRNAs associated with the oncogenic roles of SphK1 remains largely unknown. The goal of this study is to detect the global gene and microRNA (miRNA) expression in response to Sphk1 over-expression and identify potential therapeutic targets. To achieve this, SphK1 was stably overexpressed in papillary thyroid cancer cell line TPC1. Then the mRNA and miRNA expression were quantified using digital gene expression (DGE) analysis and small RNA-seq in TPC1-Vector and TPC1-SphK1 cells, respectively. miRNA-mRNA interactions were explored by microT-CDS and the predicted networks were visualized using CytoScape. In this study, we found that over-expression of SphK1 differentially regulates 46 miRNA and 506 mRNAs expression in TPC1 cells. Combining bioinformatics prediction of mRNA targets and DGE data on mRNA expressions allowed to identify mRNA targets of deregulated miRNAs. The direct interaction between miR-144-3p and FN1 mRNA, which mediates the pro-invasive role of SphK1 in thyroid cancer cells, was experimentally validated. In general, our results provided a miRNA-mRNA regulatory network in response to SphK1 overexpression in thyroid cancer cells. We also demonstrated a role of miR-144-3p and FN1 in mediating oncogenic function of SphK1, which enhance the understanding of etiology of thyroid cancer.
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