Long noncoding RNA expression profiles analysis in GBM patient-derived cells stimulated with interferon gamma
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ABSTRACT:
PROVIDER: PRJNA565586 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10121035_1.fastq.gz | Fastqsanger.gz | |||
| SRR10121035_2.fastq.gz | Fastqsanger.gz | |||
| SRR10121036_1.fastq.gz | Fastqsanger.gz | |||
| SRR10121036_2.fastq.gz | Fastqsanger.gz | |||
| SRR10121037_1.fastq.gz | Fastqsanger.gz |
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Project description:Long noncoding RNAs (lncRNAs) are key regulators of gene expression both in physiological and pathological conditions. Previous studies showed changes in lncRNA expression during tumorigenesis. To analyze the role of lncRNAs in tumor interferon signaling and cancer-mediated immunosuppression, we used RNA-seq technique to identify lncRNAs that are differentially expressed in GBM patient-derived cells stimulated with interferon gamma compared to unstimulated cells. 15,768 lncRNAs were surveyed in the analysis. RNA-seq data show upregulation of 113 lncRNAs upon interferon gamma treatment (p value < 0.01, fold change > 2). Our findings indicate that the expression of several lncRNAs is stimulated by interferon gamma suggesting a critical role of lncRNAs in tumor interferon signaling.
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Project description:Tumor interferon signaling regulates the expression of immunosuppressive molecules and promotes cancer immune evasion. Although the role of long noncoding RNAs (lncRNAs) in the regulation of gene expression is now emerging, their function in tumor interferon signaling remains unexplored. We have identified the interferon-γ (IFNγ)-stimulated non-coding RNA 1 (INCA1) as a novel lncRNA expressed form the PD-L1 locus. INCA1 is expressed in multiple tumor types and its levels increase after IFNγ stimulation. In this study we performed transcriptome analysis (RNA-seq) of INCA1 knockdown cells and show that INCA1 regulates the expression of several interferon-stimulated genes. Overall, our findings reveal INCA1 as a critical component of the tumor interferon signaling.
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Project description:Tumor interferon signaling regulates the expression of immunosuppressive molecules and promotes cancer immune evasion. Although the role of long noncoding RNAs (lncRNAs) in the regulation of gene expression is now emerging, their function in tumor interferon signaling remains unexplored. We have identified the interferon-γ (IFNγ)-stimulated non-coding RNA 1 (INCA1) as a novel lncRNA expressed form the PD-L1 locus. INCA1 is expressed in multiple tumor types and its levels increase after IFNγ stimulation. Silencing INCA1 decreased the expression of several interferon-stimulated genes (ISGs). We discovered that the transcripts of some ISGs are negatively regulated by HNRNPH1. We demonstrate that binding of INCA1 to HNRNPH1 is required for ISG expression. Overall, our findings reveal a mechanism of tumor interferon signaling regulation mediated by the lncRNA INCA1.
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Project description:Toxoplasma strains are known to inhibit the expression of several interferon-gamma induced genes, and a type II strain was shown to dysregulate genome-wide responses to interferon-gamma in human fibroblasts (Kim et al., 2007, J Immunol.). In this study we aimed to determine the effect of infection with three clonal lineages of Toxoplasma, type I, II, and III strains on genome-wide interferon-gamma induced transcription in murine macrophages. We also assessed the effect of the two main Toxoplasma modulators of mouse macrophage transcription, ROP16 and GRA15 (Jensen et al., 2011, Cell Host Microbe). We used Affymetrix microarrays to analyze host cell transcription after Toxoplasma infection and interferon-gamma stimulation. RAW264.7 murine macrophages were left uninfected or infected with type I (RH), type I ?rop16 (RH ?rop16), type II (Pru), type II ?gra15 (Pru ?gra15), or type II (CEP) parasites at an MOI ~5 for 18 hours and subsequently stimulated with murine IFN-? for six hours. Plaque assays were done to assess parasite viability. Total RNA was isolated and hybridized to Affymetrix Mouse 430A 2.0 gene chips.
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