Inflammatory response to IL-1b in WT, LDHA KO, NAMPT KO, NFKBIZ KO and FX11 treated chondrocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA623356 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11487000_1.fastq.gz | Fastqsanger.gz | |||
| SRR11487000_2.fastq.gz | Fastqsanger.gz | |||
| SRR11487001_1.fastq.gz | Fastqsanger.gz | |||
| SRR11487001_2.fastq.gz | Fastqsanger.gz | |||
| SRR11487002_1.fastq.gz | Fastqsanger.gz |
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Project description:Our goal is to study the impacts of IL-1b treatment on chondrocyte physiology. Furthermore, we knocked out several genes that we believe are important for modulating the inflammatory response. We find that IL-1b treatment induces metabolic reprogramming towards aerobic glycoylsis. We found that inhibition of LDHA using inbhitiro FX11 inhibited the inflammatory response of chondrocytes. We hypothesized that this effect was mediated by interaction with NADH, leading to regulation of IkB-z protein. Thus, deletion of LDHA, NAMPT or NFKBIZ was performed and found to inhibit inflammatory response genes induced by IL-1b, with similar gene expression changes amongst the three suggesting that they may work in the same pathway.
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Project description:Constitutive activation of the nuclear factor-kappa B (NF-kB) pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Recurrent mutations of NF-kB regulators that cause constitutive activity of this oncogenic pathway have been identified. However, it remains unclear how specific target genes are regulated. We identified the IkB-like protein NFKBIZ that binds NF-kB subunits and enhances transactivation of some NF-kB target genes while repressing others, to be upregulated in ACB compared to GCB DLBCL primary patient samples (p=5.1 x 10^-37). Knockdown of NFKBIZ by RNA interference was toxic to ABC but not GCB DLBCL cell lines. Gene expression profiling following NFKBIZ knockdown significantly downregulated a large number of NF-kB target genes, suggesting a central role in regulating NF-kB signaling. To further investigate the molecular mechanisms of how NFKBIZ mediates NF-kB signaling in ABC DLBCL, we performed immunoprecipitations and detected an interaction of NFKBIZ with both p50 and p52 NF-kB subunits, indicating that both the canonical and non-canonical NF-kB pathways are regulated by NFKBIZ. Collectively, our data imply that NFKBIZ is required for NF-kB signaling in ABC DLBCL and thus might represent a promising molecular target for future therapies. The complete dataset is comprised of three experiments with the male HBL-1 ABC DLBCL cell line: a) 8 paired GEP measurements after NFKBIZ inhibition by shRNA, b) 6 paired GEP measurements after applying the MLN inhibitor and c) 4 two-color measurements after applying a MALT inhibitor.
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