Dataset Information

Long noncoding RNA expression profiles analysis in GBM patient-derived cells stimulated with interferon gamma

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137453 | GEO | 2020/07/29

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Peste des petits ruminants virus (PPRV) infection causes highly contagious and severe disease in domestic and wild ruminants. It is widely reported that PRRV infection causes considerable innate immunosuppression in its host and promotes viral replication. However, how does the host rescue the innate immune response to counteract this immunosuppression during viral replication is poorly understood. The goat fetal fibroblasts (GFFs) have been commonly used as host-original cells to investigate the pathogenesis of PPRV. To explore the mechanisms of how host counteracts PPRV-mediated innate immunosuppression, a high-throughput quantitation proteomic approach (iTRAQ in conjunction with LC-MS/MS) was used to investigate the proteome landscape of GFFs in response to PPRV infection. Eventually, the proteomic analysis gained 497 up-regulated proteins and 358 down-regulated proteins (PPRV-infected cells versus mock-infected cells). The complement and coagulation cascades, protein digestion and absorption, and cytokine-cytokine receptor interaction pathways were significantly regulated in response to PPRV infection. ErmineJ analysis of the differentially expressed proteins (DEPs) identified the significantly enriched GO categories for response to interferon-gamma and positive regulation of ERK1 and ERK2 cascade. In addition, many immune related proteins, such as interferon gamma, 2'-5'-oligoadenylate synthase-like protein, toll-like receptor 9, toll-like receptor 6, NOD1, plasminogen activator inhibitor 1, and Wnt-5a were significantly upregulated. This suggested that the innate immune response was triggered during PPRV infection in GFFs. We subsequently identified that the E3 ubiquitin ligase FANCL was critically involved in regulation of the innate immune response during PPRV infection. FANCL inhibited PPRV infection by enhancing type I interferon (IFN) and interferon-stimulated genes (ISGs) expression. Further study indicated that FANCL induced type I IFN production by promoting TBK1 phosphorylation, and therefore impairing PPRV-mediated immunosuppression and revealing an antiviral function against PPRV.

Dataset Information

Long noncoding RNA expression profiles analysis in GBM patient-derived cells stimulated with interferon gamma

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets