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ERbeta influencing p65 cistromes in colon cancer cells

ABSTRACT: ERbeta influencing p65 cistromes in colon cancer cells

PROVIDER: PRJNA674648 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12982751.fastq.gz	Fastqsanger.gz
	SRR12982752.fastq.gz	Fastqsanger.gz
	SRR12982753.fastq.gz	Fastqsanger.gz
	SRR12982754.fastq.gz	Fastqsanger.gz
	SRR12982755.fastq.gz	Fastqsanger.gz

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ERbeta influencing p65 cistromes in colon cancer cells

Project description:Inflammation is involved in both initiation and promotion of colorectal cancer (CRC), and patients with inflammatory bowel disease (IBC) have increased risk of developing CRC. Tumor necrosis factor alpha (TNFα) is a cytokine secreted by e.g. macrophages, and this signaling is deregulated in IBD and CRC. TNFα activates the pro-survival transcription factor complex NFκB, which is composed of several subunits including p65 (RELA). We recently characterized the genome-wide transcriptional impact by TNFα in two CRC cell lines, but how p65 binds the chromatin, its cistrome, in colorectal cancer cells has not been explored. We here used p65 chromatin immunoprecipitation followed by sequencing (ChIP-Seq) in HT29 and SW480 cells, and correlated with the transcriptomic impact of TNFα. Further, estrogen receptor beta (ERβ) has anti-inflammatory and anti-tumorigenic effects in colon cells and interacts with NFκB main targets. We have shown that ERβ impacts TNFα signaling in CRC cells and ERβ impacts the P65 cistrome.

2021-03-01 | GSE160856 | GEO

p65

Project description:p65

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ERbeta modulation of NFkB pathway in colon cancer cell lines SW480 and HT29

Project description:Analysis of differentially expressed genes in colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours. Total RNA obtained from colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours.

2016-07-17 | E-GEOD-65979 | biostudies-arrayexpress

ERbeta modulation of NFkB pathway in colon cancer cell lines SW480 and HT29

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siRNA knockdown screening of possible NF-kB p65 interactors influencing IL-1-NF-kB gene expression

Project description:The transcription factor NF-κB p65 plays a key role in innate and adaptive immunity. It functions as a master regulator of the inflammatory response by inducing the expression of pro-inflammatory genes including secreted cytokines (IL6), chemokines (IL8, CXCL2), and multiple regulatory intracellular proteins (NFKBIA). NF-κB is activated by the so-called canonical, noncanonical and atypical signalling pathways. In the canonical pathway, activation of the Interleukin-1 receptor complex triggers degradation of the cytosolic p65 inhibitor IBα followed by nuclear translocation of p65 where it is directed by unknown pathways to the enhancers and promoters of pro-inflammatory genes. Despite its pleiotropic functions in adaptive and innate immunity or stress reactions, the entire repertoire of p65 interacting factors that contribute to its general or stimulus-specific functions within the nucleus or other cell compartments is still elusive. We identified the p65 interactomes in intact cells by BioID pulldowns under inflammatory condition (+IL-α). Extensive bioinformatics analysis of the proximity labeling data sets revealed several hundred high confidence interactors including multiple novel factors that have not been reported in the literature. We investigated which of our 38 high-confidence interactors have an impact on IL-1 NF-kB gene expression by siRNA screening. We found 5 interesting hits in the context of inflammation which will be further assessed by microarray analysis.

2025-03-05 | GSE244637 | GEO

siRNA knockdown screening of possible NF-kB p65 interactors influencing IL-1-NF-kB gene expression

Project description:siRNA knockdown screening of possible NF-kB p65 interactors influencing IL-1-NF-kB gene expression

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Myeloid cell RelA/p65 promotes lung cancer proliferation

Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).

2012-03-31 | E-GEOD-36568 | biostudies-arrayexpress

Colon cancer

Project description:Colon cancer

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Project description:Colon cancer

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Project description:Nuclear factor kappa B (NF-κB) is a central regulator of inflammation, infection, and immunity pathways and is often dysregulated in autoimmune diseases, inflammatory disorders, and cancers. However, the mechanisms by which different stimuli, including cellular metabolism, modulate NF-κB activation remain unclear. Here, we report that RelA ( p65), a major component of NF-κB, is S-palmitoylated at cysteine 197 and 206 by directly reacting with palmitoyl-CoA. Autopalmitoylation of p65 promotes its nuclear localization and p65-p50 complex formation, thereby enhancing NF-κB transcriptional activities. Furthermore, p65 palmitoylation upregulates RelB expression and promotes non-canonical NF-κB complex formation, further amplifying pathway activation. We also demonstrate that a high-fat diet could enhance p65 palmitoylation and correlate with an increased cytokine production in mouse tissues. These results reveal that lipid metabolism might directly regulate NF-κB activity and suggest that targeting p65 auto-palmitoylation could be a potential therapeutic strategy for diseases with deregulated NF-κB pathway.

2025-01-17 | GSE286561 | GEO

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