IRF2BP2 promotes neuroblastoma progression
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ABSTRACT:
PROVIDER: PRJNA990742 | ENA |
REPOSITORIES: ENA
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Project description:We report a previously unrecognized role of IRF2BP2 in neuroblastoma. To explore IRF2BP2-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the IRF2BP2-knockdown SK-N-BE(2) cells in comparison to control group. We find that IRF2BP2 contributes to maintenance ADRN signature of neuroblastoma cell.
2024-06-24 | GSE236390 | GEO
Project description:MYCN and SOX11 are master transcription factors (TFs) in neuroblastoma by directly occupying each other's and their own super-enhancers (SEs). Additionally, Master TFs cooperatively co-occupy the same SE components, which promotes the expression of IRF2BP2 involved in cell survival. We also observed the significant enrichment of the AP-1 family at the binding sites of IRF2BP2. In the present study, CUT&Tag (Cleavage Under Targets and Tagmentation) analysis was performed to explore the target of IRF2BP2, MYCN, AP-1 and SOX11 in NB cells.
2024-06-24 | GSE246065 | GEO
Project description:IRF2BP2 Modulates Chromatin Accessibility in Neuroblastoma
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Project description:Super-enhancer-associated TTC8 promotes neuroblastoma progression
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Project description:Chromatin accessibility of SK-N-BE(2) cells without or with IRF2BP2 depletion were profiled using transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) to identify potential regulatory elements.
2024-06-24 | GSE246063 | GEO
Project description:SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7
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Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of cell-intrinsic inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that IRF2BP2 interacts with the AP-1 heterodimer ATF7/JDP2, which is involved in activating inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene-activating function. Loss of IRF2BP2 leads to overactivation of inflammatory pathways, resulting in strongly reduced proliferation. Our research indicates that a precise equilibrium between activating and repressive transcriptional mechanisms creates a pro-oncogenic inflammatory environment in AML cells. The ATF7/JDP2-IRF2BP2 regulatory axis is likely a key regulator of this process and may, therefore, represent a promising therapeutic vulnerability for AML. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.
2024-05-07 | GSE229594 | GEO
Project description:Knocking down IRF2BP2 led to decreased T-cell acute lymphoblastic leukemia (T-ALL) cell survival and growth both in vitro and in vivo. To explore IRF2BP2-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the IRF2BP2-knockdown J.gamma1 cells in comparison to control group. Cleavage Under Targets and Tagmentation (CUT&Tag) showed the co-localization of IRF2BP2 with several master transcription factors on chromatin in J.gamma1 cells.
2024-10-26 | GSE267451 | GEO
Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by the abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator that has been implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that in AML cells IRF2BP2 interacts with the transcriptional heterodimer ATF7/JDP2, which is involved to activate inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene activating function. Loss of IRF2BP2 leads to the overactivation of inflammatory pathways, resulting in immediate cell death. Our findings suggest that a delicate balance of activating and repressive transcriptional mechanisms establishes a pro-oncogenic inflammatory set-up in AML cells, and that manipulation of the ATF7/JDP2-IRF2BP2 regulatory axis may offer a potential vulnerability for AML treatment. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.
2024-05-16 | PXD041817 | Pride
Project description:Previous studies have reported that metastatic tumor cells acquire genomic aberrations compared to those present in the primary due to an unstable genome. However, it is not clear if all malignancies follow a similar pattern. Neuroblastoma is the most common extra-cranial solid tumor of childhood. To examine how the neuroblastoma genome changes during tumor progression, we investigated chromosomal structural alterations across three tumors from a patient with hisg-risk neuroblastoma. The tumors included the primary tumor, one metastatis collected at diagnosis before any treatment, and a second metastatis collected during post mortem investigation. The recapitulated chromosomal structural alterations demonstrated that all three tumors had extensive chromosomal alterations involving virtually every chromosome. All tumors were aneuploid and shared many chromosomal alterations often seen in neuroblastoma. Despite some tumor to tumor structural variability, approximately 81-91% of the altered regions were shared among the three tumor genomes with primary tumor and pre-treamment metastatis being the most similar. Three samples from one patient with high-risk neuroblastoma. Primary tumor plus two metastatic tumors. One of metastasis sampled at diagnosis, before any treatment, and second metastasis taken at autopsy.
2011-12-01 | E-GEOD-33987 | biostudies-arrayexpress