Propagated circulating tumor cells uncover the role of NF-kB and COP1 in metastasis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA879720 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21533715_1.fastq.gz | Fastqsanger.gz | |||
| SRR21533715_2.fastq.gz | Fastqsanger.gz | |||
| SRR21533716_1.fastq.gz | Fastqsanger.gz | |||
| SRR21533716_2.fastq.gz | Fastqsanger.gz | |||
| SRR21533717_1.fastq.gz | Fastqsanger.gz |
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Project description:The nuclear factor kB (NF-kB) subunits RelA, RelB, c-Rel, p50 and p52 are each critical for B-cell development and function. To systematically characterize their responses to canonical and non-canonical NF-kB pathways activity, we performed ChIP-seq analysis in lymphoblastoid B-cells. We found a surprisingly complex NF-kB binding landscape, which did not readily reflect the two NF-kB pathway paradigm. Instead, ten subunit binding patterns were observed at promoters and eleven at enhancers. Surprisingly, nearly one-third of NF-kB binding sites lacked kB motifs. De novo motif finding uncovered distinct modes of NF-kB recruitment at these sites. The oncogenic forkhead box protein FOXM1 and NF-kB co-occupied many kB sites despite the absence of a FOXM1 DNA motif. FoxM1 knockdown decreased expression of key NF-kB targets and caused apoptosis. Our study highlights opportunities for selective therapeutic NF-kB blockade.
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