NFKB2 Knockdown Reduces Expression of HR-Related Genes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA624857 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11539048.fastq.gz | Fastqsanger.gz | |||
| SRR11539049.fastq.gz | Fastqsanger.gz | |||
| SRR11539050.fastq.gz | Fastqsanger.gz | |||
| SRR11539051.fastq.gz | Fastqsanger.gz | |||
| SRR11539052.fastq.gz | Fastqsanger.gz |
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Project description:This study systematically analyzed the molecular mechanism and function of nuclear factor kappa B subunit 2 (NFKB2) in colorectal cancer (CRC) to investigate the potential of NFKB2 as a therapeutic target for CRCTo investigate the potential of NFKB2 as a therapeutic target for colorectal cancer (CRC), we conducted a systematic analysis of the molecular mechanism and function of NFKB2 in CRC. VariousA range of experimental techniques, including RNA sequencing, proteome chip assays, and small molecule analysis, were used to obtaingain a deeper understanding of the regulation of NFKB2 in CRC. TheOur results revealed that NFKB2 was upregulated in a significant proportion of patients with advanced hepatic metastasismetastases of CRC. NFKB2 played an importanta role in promoting tumor growth through CD8+ T cell exhaustion. MoreoverAdditionally, NFKB2 directly interacted with signal transducer and activator of transcription 2 (STAT2)STAT2, leading to increased phosphorylation of STAT2 and the upregulation of programmed death ligand 1 (PD-L1)PD-L1 expression. Applying aThe application of a small molecule inhibitor of NFKB2 (Rg5) led to a reduction in PD-L1 expression and improved response to programmed death-1 (PD-1)PD-1 blockade-based immunotherapy. In conclusion,These findings suggest that the facilitated NFKB2-STAT2/PD-L1 axis may suppresses immune surveillance in CRC and targeting NFKB2 maycould enhance the efficacy of immunotherapeutic strategies. Our resultsThis study provides novel insights into the molecular mechanisms underlying the contribution of NFKB2 in CRC immune escape. However, our findings requireand further validation of these findings in a clinical trial is needed to establish NFKB2 inhibition as a therapeutic strategy for CRC patients.
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Project description:As such, TNF triggers the canonical NF-?B pathway to induce a nuclear NF-?B activity composed of the RelA:p50 dimer in WT cells. Nfkb2 encodes p100, which regulates the activity of the RelB NF-?B heterodimers during immune cell-differentiation via the noncanonical pathway. Our biochemical analyses revealed that an absence of p100 instead repositions RelB under the control of the TNF-activated canonical pathway. Indeed, chronic TNF treatment of Nfkb2-/- cells activates the RelA:p50 dimer and an additional RelB:p50 dimer. On the other hand, TNF stimulation of Relb-/-Nfkb2-/- and Rela-/-Nfkb2-/- MEFs exclusively activated the RelA:p50 dimer and the RelB:p50 dimer, respectively. We treated this panel of knockout MEFs with TNF for 6h before being subjected to microarray mRNA analysis. We also included in our analysis WT MEFs and Rela-/-Relb-/-Rel-/- MEFs, which served as a negative control. Our analyses revealed overlapping and distinct gene-expression specificities of RelA:p50 and RelB:p50 dimers activated in mutant cells in response to TNF.
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Project description:We report the application of ChIP-Seq analysis for high-throughput profiling of NFKB2/p52 binding pattern under prolonged culture conditions. Briefly, we investigate the genome wide binding behavior of endogenous p52 in WI-38 cells. The cells was cultured with regular DMEM medium for prolonged time (7 days). Chromatin immunoprecipitated DNA was converted to libraries for sequencing with HiSeq 4000. We find that there is a distinct binding pattern of p52 under prolonged culture condtion. This study provides a preliminary but solid basis to our understanding of NFKB2/p52 binding dynamics during aging process.
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