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Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex

ABSTRACT: HTLV-1 is an onco-retrovirus that infects human T cells and causes poor prognosis leukaemia/lymphoma, ATL. The viral RNA binding protein, Rex, intervenes in host cell regulation of gene expression, splicing and translation mechanisms to promote viral particle replication, but the detailed mechanism of its function has not been elucidated. In the present study, we stably overexpressed HTLV-1 Rex in the human T-cell-derived cell line, CEM, and investigated effect of Rex on splicing patterns in CEM cells by exon microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193574 | GEO | 2022/03/03

REPOSITORIES: GEO

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Human gene expression microarray analysis in CEM cells overexpressing HTLV-1 Rex

Project description:HTLV-1 is an onco-retrovirus that infects human T cells and causes poor prognosis leukaemia/lymphoma, ATL. The viral RNA binding protein, Rex, intervenes in host cell regulation of gene expression, splicing and translation mechanisms to promote viral particle replication, but the detailed mechanism of its function has not been elucidated. In the present study, we stably overexpressed HTLV-1 Rex in the human T-cell-derived cell line, CEM, and investigated effect of Rex on gene expression profiles in CEM cells by gene expression microarray analysis.

2022-03-03 | GSE193576 | GEO

Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex

Project description:Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex

| PRJNA796617 | ENA

Human gene expression microarray analysis in CEM cells overexpressing HTLV-1 Rex

Project description:Human gene expression microarray analysis in CEM cells overexpressing HTLV-1 Rex

| PRJNA796615 | ENA

Intragenic recruitment of NF-kB drives splicing modifications upon activation by the oncogene Tax of HTLV-1

Project description:Chronic NF-kB activation in inflammation and cancer has long been linked to persistent activation of NF-kB–responsive gene promoters. However, NF-kB factors also massively bind to gene bodies. Here, we demonstrate that recruitment of the NF-kB factor RELA to intragenic regions regulates alternative splicing upon NF-kB activation by the viral oncogene Tax of HTLV-1. Integrative analyses of RNA splicing and chromatin occupancy, combined with chromatin tethering assays, demonstrate that DNA-bound RELA interacts with and recruits the splicing regulator DDX17, in an NF-kB activation–dependent manner. This leads to alternative splicing of target exons due to the RNA helicase activity of DDX17. Similar results were obtained upon Tax-independent NF-kB activation, indicating that Tax likely exacerbates a physiological process where RELA provides splice target specificity. Collectively, our results demonstrate a physical and direct involvement of NF-kB in alternative splicing regulation, which significantly revisits our knowledge of HTLV-1 pathogenesis and other NF-kB–related diseases.

2020-05-12 | GSE123752 | GEO

Phaeocystis rex

Project description:Phaeocystis rex overview

| PRJNA535357 | ENA

Rhinolophus rex

Project description:Rhinolophus rex overview

| PRJNA436433 | ENA

Thymic Epithelial Cells with Human T cell Leukemia Virus type 1 (HTLV-1) Infected T cell supernatant (CEM, CIB, C91PL)

Project description:The human T-lymphotropic virus type-1 (HTLV-1) is the cause of adult T cell leukemia/lymphoma (ATL) and HTLV-1 associated myelopathy/tropical spatic paraparesis (HAM/TSP). Both diseases have a late onset, although ATL has a medium survivor of 7.7 months after the onset despise aggressive treatment. T CD4+ cells are the main target of HTLV-1, but other cells types are known to be infected as T CD8+, CD34+ progenitor, dendritic cells and immature lymphocytes. The thymus gland is a primary lymphoid organ, in which the lymphocytes undergo differentiation, where selected T cell ultimately being exported from the organ and going to peripheral lymphoid organs. This process occurs along with immature lymphocyte migration and interaction with thymic microenvironment. Thymic epithelial cells (TECs) are the main component of the thymic stroma and are responsible for the process of intrathymic T cell maturation. This process are dependent of T cell receptor (TCR)-mediated recognition of antigenic peptide fragments presented by major histocompatibility complex (MHC) molecules in TEC and culminate in TCR repertoire formation. In this study, we show that TECs have the receptors for HTLV-1 entry and can be infected by cell-cell contact and cell-free virus. These cells change gene expression of anti-apoptosis, chemokine and adhesion molecules genes; however, there is no difference in antigen presentation molecules. Furthermore, HTLV-1 infected TECs can transmit the virus to a CD4 T cell lineage and CD4 T cells derived from peripheral blood of healthy donors after in vitro co-cultivation. Conjointly, our data points to the possibility that the human thymic epithelial cells must favor the HTLV-1 infection as a reservoir, transmitting the virus to maturing lymphocytes that cause the disease in the periphery.

2015-11-30 | GSE73169 | GEO

Gene expression profiling of interferon-alpha-treated HTLV-1-infected CD4+ T cell lines

Project description:Background: Interferon-alpha (IFN-a) contributes extensively to the host immune response upon viral infection through antiviral, pro-apoptotic, antiproliferative and immunomodulatory activities. Although extensively documented in various types of human cancers and viral infections, controversy exists in the exact mechanism of action of IFN-a in human immunodeficiency virus type 1 (HIV-1) and human T lymphotropic virus type 1 (HTLV-1) retroviral infections. Principal Findings: IFN-a displayed robust anti-HIV-1 effects in HTLV-1/HIV-1 co-infected MT-4 cells in vitro, demonstrated by the dose-dependent inhibition of the HIV-1-induced cytopathic effect (IC50 = 83.5IU/ml, p < 0.0001) and p24 secretion (IC50 = 1.2 IU/ml, p < 0.0001). In contrast, IFN-a treatment did not affect cell viability nor HTLV-1 viral RNA levels in HTLV-1 mono-infected cell lines, based on flow cytometry and nCounter analysis. However, we were able to confirm the previously described posttranscriptional inhibition of HTLV-1 p19 secretion by IFN-a, both in cell lines (p = 0.0045) as well as in adult T cell leukemia patient samples (p = 0.031). In addition, through microarray and nCounter analysis, we demonstrated significant transcriptional activation of interferon-stimulated genes and intact IFN-a signaling in HTLV-1-infected cell lines. Conclusions: Taken together, our results indicate that both the absence of in vitro antiproliferative and pro-apoptotic activity, as well as the modest posttranscriptional antiviral activity of IFN-a against HTLV-1, was not due to a cell intrinsic defect in IFN-a signalisation, but rather represents a retrovirus-specific phenomenon, considering the robust HIV-1 inhibition in co-infected cells.

2015-01-01 | GSE34870 | GEO

Human CEM Cells: Control vs. 2h or 4.5h Cluvenone Treated

Project description:Transcriptional profiling of human CEM cells comparing control untreated CEM cells with either 2h or 4.5h cluvenone-treated CEM cells.

2010-08-11 | GSE23536 | GEO

mRNA-seq analysis of rex-1 deletion in C. elegans

Project description:In embryos, DCC binding across the length of the ~17.7 Mb X chromosome initiates at a set of recruitment elements on the X (rex). Individual rex sites collectively contribute to recruitment and repression, thus deletion of one or few rex sites causes subtle changes, as measured by mRNA-seq in mixed-stage embryos. We previously constructed a strain deleting rex-1, located ~6 kb downstream of dpy-23 (https://doi.org/10.7554/eLife.23645). Here we performed mRNA-seq in rex-1 deletion embryos.

2024-04-29 | GSE265989 | GEO

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