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TNFα and LTβ stimulated UM-SCC 46 gene expression [TNF]

ABSTRACT: TNFα and LTβ stimulated UM-SCC 46 gene expression [TNF]

PROVIDER: PRJNA523626 | ENA |

REPOSITORIES: ENA

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TNFα and LTβ stimulated UM-SCC 46 gene expression [TNF]

Project description:To investigate the regulatory mechanisms and targets of the activation of NF-kB and inflammatory pathways, we treated HPV(-) head and neck cancer line UM-SCC 46 cells with TNFα and LTβ at different time points, and compared the gene expression by microarray. TNFα uniquely induced 172 genes, LTβ specifically induced 202 genes, while 155 genes were induced by both ligands. Total RNA samples were isolated from UM-SCC 46 cells after TNFα or LTβ treatment at different time points, and the gene expression were compared with untreated cell controls.

2019-02-22 | GSE126904 | GEO

TNFα and LTβ stimulated UM-SCC 46 gene expression [LTB]

Project description:To investigate the regulatory mechanisms and targets of the activation of NF-kappaB and inflammatory pathways, we treated HPV(-) head and neck cancer line UM-SCC 46 cells with TNFα and LTβ at different time points, and compared the gene expression by microarray. TNFα uniquely induced 172 genes, LTβ specifically induced 202 genes, while 155 genes were induced by both ligands. Total RNA samples were isolated from UM-SCC 46 cells after TNFα or LTβ treatment at different time points, and the gene expression were compared with untreated cell controls.

2019-02-22 | GSE126903 | GEO

TNFα and LTβ stimulated UM-SCC 46 gene expression [LTB]

Project description:TNFα and LTβ stimulated UM-SCC 46 gene expression [LTB]

| PRJNA523625 | ENA

TNFa and LTB stimulated UM-SCC 46 gene expression

Project description:TNFa and LTB stimulated UM-SCC 46 gene expression

| PRJNA523623 | ENA

Genome-wide analysis of histone modification in UPCI-SCC-090, UM-SCC-104, FaDu and NP69SV40T.

Project description:We analysed active enhancers in UPCI-SCC-090, UM-SCC-104, FaDu and NP69SV40T by performing ChIP-seq on H3K4me3, H3K4me1 and H3K27ac.

2023-01-06 | GSE211473 | GEO

Effect of MIR-375 expression on UM-SCC-1

Project description:MicroRNA mir-375 was expressed in head and neck cancer UM-SCC-1 tumor cells and expression was compared to empty vector control.

2017-03-15 | E-MTAB-5405 | biostudies-arrayexpress

Genome-wide analysis of histone modification in UPCI-SCC-090, UM-SCC-104, FaDu and NP69SV40T.

Project description:Genome-wide analysis of histone modification in UPCI-SCC-090, UM-SCC-104, FaDu and NP69SV40T.

| PRJNA870481 | ENA

Quantitative Phospho-proteomic Analysis of TNFα/NFκB Signaling Reveals a Role for RIPK1 Phosphorylation in Suppressing Necrotic Cell Death

Project description:TNFα is a potent inducer of inflammation due to its ability to promote gene expression, inpart via the NFκB pathway. Moreover, in some contexts, TNFα promotes Caspase-dependent apoptosis or RIPK1/RIPK3/MLKL-dependent necrosis. Engagement of the TNF Receptor Signaling Complex (TNF-RSC), which contains multiple kinase activities, promotes phosphorylation of several downstream components, including TAK1, IKKα/IKKβ, IκBα and NFκB. However, immediate downstream phosphorylation events occurring in response to TNFα signaling are poorly understood at a proteome-wide level. Here we use Tandem mass tagging-based proteomics to quantitatively characterize acute TNFα-mediated alterations in the proteome and phosphoproteome with or without inhibition of the cIAP-dependent survival arm of the pathway with a SMAC mimetic. We identify and quantify over 8,000 phosphorylated peptides, among which are numerous known sites in the TNF-RSC, NFκB, and MAP kinase signaling systems, as well as numerous previously unrecognized phosphorylation events. Functional analysis of S320 phosphorylation in RIPK1 demonstrates a role for this event in suppressing its kinase activity, association with CASPASE-8 and FADD proteins, and subsequent necrotic cell death during inflammatory TNFα stimulation. This study provides a resource for further elucidation of TNFα-dependent signaling pathways.

2017-05-30 | PXD006055 | Pride

TNFa and LTB stimulated UM-SCC 46 gene expression

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

2019-02-22 | GSE126905 | GEO

Targeting eRNA-producing super-enhancers regulates TNFα expression and mitigates chronic inflammation in mice and patient-derived immune cells [CUT&RUN]

Project description:Chronic inflammatory diseases are driven by immune cell dysregulation and overproduction of pro-inflammatory molecules, such as tumor necrosis factor alpha (TNFα). Super-enhancers (SEs) and their enhancer RNAs (eRNAs) are critical gene expression regulators and offer therapeutic potential beyond protein-targeting approaches. We hypothesized that targeting eRNAs could reduce chronic inflammation by modulating TNFα expression. We generated TNF-9 knockout (KO) mice by deleting a Tnfα-regulating enhancer region. These mice exhibited significantly reduced Tnfα levels, improved disease outcomes, and diminished immune cell activation in models of rheumatoid arthritis (RA), psoriasis, and lipopolysaccharide (LPS)-induced sepsis. Integrative epigenomic and transcriptomic analysis identified additional LPS-responsive, eRNA-producing enhancers as therapeutic targets. Antisense oligonucleotide (ASO)-mediated knockdown of TNF-9 eRNA in mouse macrophages demonstrated decreased Tnfα expression and alleviated RA symptoms. Furthermore, ASO-mediated inhibition of the eRNA of the human homolog of TNF-9 similarly reduced TNFα levels. These findings support eRNA-targeted interventions as potential treatment for chronic inflammatory diseases.

2025-03-11 | GSE291298 | GEO

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