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A novel IFNα-induced long noncoding RNA, lncMX1-215, negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma

ABSTRACT: A novel IFNα-induced long noncoding RNA, lncMX1-215, negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma

PROVIDER: PRJNA574925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10202338_1.fastq.gz	Fastqsanger.gz
	SRR10202338_2.fastq.gz	Fastqsanger.gz
	SRR10202339_1.fastq.gz	Fastqsanger.gz
	SRR10202339_2.fastq.gz	Fastqsanger.gz
	SRR10202340_1.fastq.gz	Fastqsanger.gz

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A novel IFNα-induced long noncoding RNA, lncMX1-215, negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma

Project description:Interferon-alpha (IFNα) plays a ciritical role in immune regulation, especially in tumor microenvironment. Our previous study has demonstrated that IFNα promoted immunosuppression formation in head and neck squamous cell carcinoma. To explore the mechanism underlying IFNα-induced immunosuppression, long noncoding RNA (lncRNA) sequece was conduted. We identified a novel IFNα-induced upregulated lncRNA, lncMX1-215 in HNSCC. It was mainly located in cell nucleus. Ectopic expression of lncMX1-215 markedly inhibited IFNα-induced immunosuppression molecules, programmed cell death 1 ligand 1(PD-L1) and galectin-9 expression, and vice versa. Subsequently, histone deacetylase (HDAC) inhibitors promoted the expression of PD-L1 and galectin-9. There were binding sites of H3K27 acetylation on PD-L1 and galectin-9 promoters. Mechanically, we find that lncMX1-215 directly interacted with GCN5, a known H3K27 acetylase to interrupt its binding to H3K27 acetylation. Clinically, negative correlations between lncMX1-215 and PD-L1, galectin-9 were observed. Finally, overexpression of lncMX1-215 suppressed the proliferation and metastasis capacity in vitro and in vivo in HNSCC. Our results suggest that lncMX1-215 negatively regulates immunosuppression through interrupting GCN5/H3K27ac in HNSCC and provides novel insights into immune checkpoint blockade treatment.

2020-01-13 | GSE138147 | GEO

A novel IFNα-induced long noncoding RNA negatively regulates immunosuppression by interrupting H3K27 acetylation in head and neck squamous cell carcinoma.

Project description:BackgroundInterferon alpha (IFNα) is a well-established regulator of immunosuppression in head and neck squamous cell carcinoma (HNSCC), while the role of long noncoding RNAs (lncRNAs) in immunosuppression remains largely unknown.MethodsDifferentially expressed lncRNAs were screened under IFNα stimulation using lncRNA sequencing. The role and mechanism of lncRNA in immunosuppression were investigated in HNSCC in vitro and in vivo.ResultsWe identified a novel IFNα-induced upregulated lncRNA, lncMX1-215, in HNSCC. LncMX1-215 was primarily located in the cell nucleus. Ectopic expression of lncMX1-215 markedly inhibited expression of the IFNα-induced, immunosuppression-related molecules programmed cell death 1 ligand 1 (PD-L1) and galectin-9, and vice versa. Subsequently, histone deacetylase (HDAC) inhibitors promoted the expression of PD-L1 and galectin-9. Binding sites for H3K27 acetylation were found on PD-L1 and galectin-9 promoters. Mechanistically, we found that lncMX1-215 directly interacted with GCN5, a known H3K27 acetylase, to interrupt its binding to H3K27 acetylation. Clinically, negative correlations between lncMX1-215 and PD-L1 and galectin-9 expression were observed. Finally, overexpression of lncMX1-215 suppressed HNSCC proliferation and metastasis capacity in vitro and in vivo.ConclusionsOur results suggest that lncMX1-215 negatively regulates immunosuppression by interrupting GCN5/H3K27ac binding in HNSCC, thus providing novel insights into immune checkpoint blockade treatment.

| S-EPMC6943933 | biostudies-literature

Epithelial miR-215 negatively modulates Th17-dominant inflammation by inhibiting CXCL12 production in the small intestine

Project description:MicroRNAs are a class of non-coding short-chained RNAs that control cellular functions by downregulating their target genes. Recent research indicates that microRNAs play a role in the maintenance of gut homeostasis. miR-215 was found to be highly expressed in epithelial cells of the small intestine; however, the involvement of miR-215 in gut immunity remains unknown. Here, we show that miR-215 negatively regulates inflammation in the small intestine by inhibiting CXCL12 production. Mice lacking miR-215 showed high susceptibility to inflammation induced by indomethacin, accompanied by an increased number of Th17 cells in the lamina propria of the small intestine. Our findings support a promising perspective of targeting miR-215 to treat inflammatory conditions in the small intestine.

2022-01-27 | GSE186708 | GEO

IFNα-mediated gene expression patterns

Project description:This SuperSeries is composed of the following subset Series: GSE17299: Direct effects of IFNα on human CD8 T cells_without any other concomitant signals GSE17301: The effect of IFNα on human CD8 T cells_with other concomitant signals Refer to individual Series

2010-07-23 | E-GEOD-17302 | biostudies-arrayexpress

Epithelial miR-215 negatively modulates Th17-dominant inflammation by inhibiting CXCL12 production in the small intestine

Project description:Epithelial miR-215 negatively modulates Th17-dominant inflammation by inhibiting CXCL12 production in the small intestine

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Sinorhizobium meliloti strain:215

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Gene expression changes with treatment of hsa-miR-215

Project description:Comparison of gene expression in pterygium fibroblast cells after 24 h treatment with hsa-miR-215 mimic or non-specific oligonucleotide control 100nM miR-215 mimic (Thermo Scientific) or non-specific control oligonucleotides are added to cultured fibroblast cells for 24 hours

2014-06-30 | E-GEOD-57296 | biostudies-arrayexpress

Gene expression profile of IFNα transgenic mice

Project description:The cause of systemic lupus erythematosus (SLE) is unknown. Interferonα (IFNα) has been suggested as a causative agent of SLE, however, it is not proven, and to what extent and how IFNα contributes to the disease is unknown. We here directly studied the contribution of IFNα to SLE by generating inducible IFNα transgenic mice which showed that conditional up-regulation of IFNα induced a typical manifestation of SLE including serum immune complex (IC), autoantibody against double stranded DNA (anti-dsDNA Ab) and the organ manifestations classical to SLE such as IC-deposited glomerulonephritis, classical splenic onion-skin lesion, and alopecia, epidermal liquefaction, positive lupus-band test of the skin. In the spleen of mice, activated effector CD4 T cells, interferonγ-producing CD8 T cells, B220+CD86+ cells and CD11c+CD86+ cells were increased, and the T cells produced increased amounts of IL-4, IL-6, IL-17 and IFNγ and decreased IL-2. In particular, activated CD3+CD4-CD8- double-negative T (DNT) cells positive for TCRαβ, B220, CD1d-teteramer, PD-1 and Helios, which produced increased amounts of IFNγ, IL-4, IL-17 and TNFα, were significantly expanded. They infiltrated into kidney and induced de novo glomerulonephritis and alopecia when transferred into naïve recipients. Thus, conditional up-regulation of IFNα is sufficient to induce SLE, and the DNT cells as expanded by IFNα are directly responsible for the organ manifestations such as lupus skin disease or nephritis.

2018-12-10 | GSE123549 | GEO

Lachnospiraceae bacterium CAG:215

Project description:Lachnospiraceae bacterium CAG:215 overview

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Investigating the transcriptional regulatory role of FBXA-215 [embryos]

Project description:We identified a Mariner transposase helix-turn-helix (HTH) DNA-binding domain that was captured in the Caenorhabditis genus by a subset of F-box genes, which we refer to as F-box A2 genes. The origin of F-box A2 genes likely occurred through a single transposase capture event, followed by an increase in copy number. We focused on fbxa-215, a F-box A2 gene highly expressed in the C. elegans germline and embryos, and that localizes to germ granules in embryos. The HTH domain of FBXA-215 is required for fertility and displays predominantly a signature of purifying selection, highlighting the importance of this domain. As the HTH domain of FBXA-215 is related to the DNA-binding HTH domain of transposases, we reasoned that FBXA-215 may bind to DNA in C. elegans and thus regulate gene expression at the transcriptional level. We performed mRNA sequencing of young adults and embryos to test this, but found no clear deregulation of protein-coding genes and transposable elements upon complete deletion of fbxa-215.

2024-12-15 | GSE251874 | GEO

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