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RNA sequencing analysis of lnc-HLX-2-7 interacting genes and pathways in medulloblastoma

ABSTRACT: To gain more insights into the functional significance of lnc-HLX-2-7, gene expression profiles were measured using D425, D425 lnc-HLX-2-7 KD and their intracranial xenografts by RNA sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151810 | GEO | 2020/10/30

REPOSITORIES: GEO

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Single cell RNA sequencing analysis of lnc-HLX-2-7 knock out in medulloblastoma

Project description:To gain more insights into the functional significance of lnc-HLX-2-7, gene expression profiles were measured using D425, D425 lnc-HLX-2-7 KD and their intracranial xenografts by RNA sequencing. Dissociated tumor cells were used for gel bead emulsion (GEM) with chromium controler (10X genomics).

2020-10-30 | GSE156043 | GEO

RNA sequencing analysis of intracranial D425 xenografts treated with ASO-CTRL and ASO-lnc-HLX 2-7

Project description:To gain more insights into the functional significance of lnc-HLX-2-7, gene expression profiles were measured using D425 (sh-CTRL), D425 (sh-HLX) and intracranial D425 xenografts treated with ASO-CTRL and ASO-lnc-HLX 2-7 by RNA sequencing.

2023-11-01 | GSE188746 | GEO

Genomic maps of lnc-HLX-2-7 occupancy in human medulloblastoma cell line.

Project description:To gain more insights into the functional significance of lnc-HLX-2-7 in human medulloblastoma, genomic mapping of lnc-HLX-2-7 occupancy were analyzied by ChIRP DNA sequencing.

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RNA sequencing analysis of lnc-HLX-2-7 interacting genes and pathways in medulloblastoma

Project description:RNA sequencing analysis of lnc-HLX-2-7 interacting genes and pathways in medulloblastoma

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Single cell RNA sequencing analysis of lnc-HLX-2-7 knock out in medulloblastoma

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Genes upregulated by HLX

Project description:HLX was found as a VEGF-A induced gene in HUVEC (B.Schweighofer, submitted). In order to detect genes regulated by HLX HUVEC were infected by recombinant adenovirus expressing HLX for 4, 8, 16 and 32h. RNA was isolated and subjected to microarray analysis using Affymetrix microarray. HUVEC were infected with a MOI of 40 with either HLX expressing or empty adenovirus for 4, 8, 16 or 32 hours. HUVEC without an adenovirus infection were used as control.Total RNA was isolated with Trizol according to the instructions of the manufacturer. Gene expression was analysed with Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays according to the Affymetrix protocol.

2011-02-15 | E-GEOD-13054 | biostudies-arrayexpress

Genes upregulated by HLX

2011-02-15 | GSE13054 | GEO

Identification of differentially regulated genes upon overexpression of HLX in wild-type hematopoietic stem cells

Project description:The goal was to study the role of Hlx in hematopoiesis. Sorted Lin-Kit+Sca-1+ cells from wild-type FVB/nJ bone marrow were infected with control (pCAD-IRES-GFP) or Hlx lentivirus (pCAD-IRES-GFP-Hlx) and cultured for 2 days in Iscove’s modified Dulbecco’s medium (IMDM) containing FBS, mIL-3, mIL-6 and mSCF with lentiviral supernatants in the presence of 8ug/ml polybrene. Subsequently, GFP+ cells were sorted by FACS and RNA was prepared. Three replicates of each, control vector transduced and HLX-transduced cells were used.

2012-09-14 | E-GEOD-27938 | biostudies-arrayexpress

lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

2018-11-07 | PXD011577 | Pride

Epstein-Barr Virus (EBV) activates NKL homeobox gene HLX in DLBCL

Project description:NKL homeobox genes encode developmental transcription factors regulating basic processes in cell differentiation. According to their physiological expression pattern in early hematopoiesis and B-cell development, particular members of this homeobox gene subclass constitute an NKL-code. These B-cell specific genes generate a regulatory network and their deregulation is implicated in B-cell lymphomagenesis. Epstein-Barr virus (EBV) infects B-cells and influences the activity of signalling pathways including JAK/STAT and several genes encoding developmental regulators. Therefore, EBV-infection impacts the pathogenesis and the outcome of B-cell malignancies including Hodgkin lymphoma and diffuse large B-cell lymphoma (DLBCL). Here, we isolated EBV-positive and EBV-negative subclones from the DLBCL derived cell line DOHH-2. These subclones served as model to investigate the role of EBV in deregulation of the B-cell specific NKL-code members HHEX, HLX, MSX1 and NKX6-3. We showed that the EBV-encoded factors LMP1 and LMP2A activated the expression of HLX via STAT3. HLX in turn repressed NKX6-3, SPIB and IL4R which normally mediate plasma cell differentiation. In addition, HLX repressed pro-apoptotic factor BCL2L11/BIM supporting cell survival. Thus, EBV aberrantly activated HLX thereby disturbing both B-cell differentiation and apoptosis in DLBCL. The results of our study contribute to better understand the pathogenic role of EBV in B-cell malignancies.

2019-05-06 | GSE125420 | GEO

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