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DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes [ChIP-Seq]

ABSTRACT: DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes [ChIP-Seq]

PROVIDER: PRJNA739721 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14872453.fastq.gz	Fastqsanger.gz
	SRR14872454.fastq.gz	Fastqsanger.gz
	SRR14872455.fastq.gz	Fastqsanger.gz
	SRR14872456.fastq.gz	Fastqsanger.gz
	SRR14872457.fastq.gz	Fastqsanger.gz

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DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes [microarray]

Project description:Long noncoding RNAs (lncRNAs) are deeply involved in cancer development, and we have previously reported that DLEU1 (deleted in lymphocytic leukemia 1) is frequently overexpressed in oral squamous cell carcinoma (OSCC) cells, where it plays an oncogenic role. In this study, we aimed to further clarify the molecular function of DLEU1 in the pathogenesis of OSCC. Chromatin immunoprecipitation-sequencing (ChIP-seq) analysis revealed that knockdown of DLEU1 induced substantial changes in the levels of histone H3 lysine 4 trimethylation (H3K4me3) and H3K27 acetylation (H3K27ac) in OSCC cells. Notably, depletion of DLEU1 significantly downregulated levels of H3K4me3/H3K27ac and expression of a number of interferon-stimulated genes (ISGs) including IFIT1, IFI6 and OAS1, while ectopic DLEU1 expression activated these genes. Western blot analysis and reporter assay suggested that DLEU1 upregulates ISGs through activating the JAK-STAT signaling in OSCC cells. Moreover, IFITM1, one of the ISGs induced by DLUE1, is frequently overexpressed in primary OSCC tumors, and knockdown of IFITM1 attenuated OSCC cell proliferation, migration and invasion. Our data suggest that DLEU1 exerts its oncogenic function through, at least in part, activating a series ISGs in OSCC cells.

2021-09-12 | GSE178608 | GEO

DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes [ChIP-Seq]

2021-09-12 | GSE178611 | GEO

DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes

Project description:DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes

| PRJNA739720 | ENA

DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes [microarray]

Project description:DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes [microarray]

| PRJNA739714 | ENA

Effects of DLEU1 knockdown on gene expression profiles in oral squamous cell carcinoma cells

Project description:We identified DLEU1 as a long noncoding RNA (lncRNA) frequently overexpressed in oral squamous cell carcinoma (OSCC). Knockdown of DLEU1 suppressed proliferation, migration and invasion and induced cell cycle arrest and apoptosis in OSCC cells. To further clarify the molecular function of DLEU1, we carried out gene expression microarray analysis in OSCC cell lines with DLEU1 knockdown. We found that genes associated with “matrix metalloproteinases”, “apoptosis”, “cell cycle” and “MAPK signaling” were enriched among the affected genes. These results suggest that DLEU1 may play a role in the development of OSCC.

2018-09-23 | GSE108851 | GEO

DLEU1 promotes oral squamous cell carcinoma progression by activating interferon-stimulated genes.

Project description:Long noncoding RNAs (lncRNAs) are deeply involved in cancer development. We previously reported that DLEU1 (deleted in lymphocytic leukemia 1) is one of the lncRNAs overexpressed in oral squamous cell carcinoma (OSCC) cells, where it exhibits oncogenic activity. In the present study, we further clarified the molecular function of DLEU1 in the pathogenesis of OSCC. Chromatin immunoprecipitation-sequencing (ChIP-seq) analysis revealed that DLEU1 knockdown induced significant changes in the levels of histone H3 lysine 4 trimethylation (H3K4me3) and H3K27 acetylation (H3K27ac) in OSCC cells. Notably, DLEU1 knockdown suppressed levels of H3K4me3/ H3K27ac and expression of a number of interferon-stimulated genes (ISGs), including IFIT1, IFI6 and OAS1, while ectopic DLEU1 expression activated these genes. Western blot analysis and reporter assays suggested that DLEU1 upregulates ISGs through activation of JAK-STAT signaling in OSCC cells. Moreover, IFITM1, one of the ISGs induced by DLUE1, was frequently overexpressed in primary OSCC tumors, and its knockdown inhibited OSCC cell proliferation, migration and invasion. These findings suggest that DLEU1 exerts its oncogenic effects, at least in part, through activation of a series ISGs in OSCC cells.

| S-EPMC8516910 | biostudies-literature

DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-12 | GSE178613 | GEO

Interferon-stimulated gene expression in STAT1 knockout cells

2016-07-22 | GSE84693 | GEO

Interferon-stimulated gene expression in STAT1 knockout cells

Project description:STAT1 plays a cental role in the induction of interferon-stimulated genes, but interferon alpha can activate a STAT1-independent pathway that leads to gene expression. We performed microarray analysis to examine whether like interferon alpha, interferon lambda, a newly discovered interferon, can induce the expression of interferon-stimulated genes in the absence of STAT1. Control and STAT1 knockout Huh-7.5 hepatoma cells were left untreated or treated with 1000 U/ml of human interferon alpha 2a or interferon lambda 1 (PBL) for 24 h, and total RNA was extracted. Sense-strand DNA was generated from 200 ng of total RNA, fragmented, and labeled using a GeneChip WT Plus Reagent Kit (Affymetrix). Six samples were obtained and each sample was anlyzed using one GeneChip.

2016-07-22 | E-GEOD-84693 | biostudies-arrayexpress

Fibromodulin FMOD promotes oral squamous cell carcinoma via activating EGFR signaling axis

Project description:Fibromodulin FMOD promotes oral squamous cell carcinoma via activating EGFR signaling axis

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