Transcriptional profiling of SUDHL4 cells edited by CRISPR-cas9 to induce point mutations in the FOXO1 locus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA601648 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10902618.fastq.gz | Fastqsanger.gz | |||
| SRR10902619.fastq.gz | Fastqsanger.gz | |||
| SRR10902620.fastq.gz | Fastqsanger.gz | |||
| SRR10902621.fastq.gz | Fastqsanger.gz | |||
| SRR10902622.fastq.gz | Fastqsanger.gz |
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Project description:The transcription factor FOXO1 directs germinal center (GC) polarity and supports affinity maturation by silencing immune activation programs in GC B cells. Recurrent somatic mutations in GC-derived B cell non-Hodgkin lymphomas (B-NHL) often target and reportedly activate FOXO1 by preventing its negative regulation by PI3K. Herein, using ad hoc mouse models, engineered cell lines and primary tumor specimens, we show instead that FOXO1 mutant proteins display altered transcriptional activities suggestive of partial loss-of-function. These defects drive simultaneous hyperactivation of signaling pathways (Stress Activated Protein Kinase -SAPK/JNK, Phosphoinositide 3-kinase -PI3K/AKT) and gene expression programs typically activated in GC B cells upon positive selection. Such changes confer mutant B cells with competitive advantages in response to key immune signals, leading to abnormal amplification of GC responses. Evidence of these FOXO1 ‘mutant’ gene programs can be found in a fraction of human B-NHL and predict clinical outcome, thus implying the frequent co-option of positive selection programs during GC-derived B-NHL pathogenesis.
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Project description:Mapping of WT FOXO1 and M1L FOXO1 binding sites in SUDHL4 cells
| PRJNA601647 | ENA
Project description:The transcription factor FOXO1 directs germinal center (GC) polarity and supports affinity maturation by silencing immune activation programs in GC B cells. Recurrent somatic mutations in GC-derived B cell non-Hodgkin lymphomas (B-NHL) often target and reportedly activate FOXO1 by preventing its negative regulation by PI3K. Herein, using ad hoc mouse models, engineered cell lines and primary tumor specimens, we show instead that FOXO1 mutant proteins display altered transcriptional activities suggestive of partial loss-of-function. These defects drive simultaneous hyperactivation of signaling pathways (Stress Activated Protein Kinase -SAPK/JNK, Phosphoinositide 3-kinase -PI3K/AKT) and gene expression programs typically activated in GC B cells upon positive selection. Such changes confer mutant B cells with competitive advantages in response to key immune signals, leading to abnormal amplification of GC responses. Evidence of these FOXO1 ‘mutant’ gene programs can be found in a fraction of human B-NHL and predict clinical outcome, thus implying the frequent co-option of positive selection programs during GC-derived B-NHL pathogenesis.
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Project description:We report a preliminary RNA-Seq data of MCF-7 cells edited in the FASN locus using CRISPR/Cas9. MCF-7 cells were edited by CRISPR/Cas9, screened by Surveyor assay, purified by limiting dilutions, validated by sanger sequencing, and characterized by diverse cellular analyses. Then, RNA from edited cells and non-edited controls were processed by TruSeq-RNA-Library-Prep-Kit and sequenced in a illumina equipment. Reads were aligned to hg38 in Galaxy using RNA-Star and transcripts were counted by FeatureCounts.
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Project description:Recently, the existence of extracellular miRNAs enclosed in exosomes has raised the possibility that they play an important role in cell-cell communication. To gain more insight into cell-cell communication via exosomal miRNAs, we investigated whether or not tumor cells exposed to hypoxia secrete exosomes which may affect angiogeneic activity. We used SUDHL4 cells, as donor cells, and HUVECs as recipient cells. Exosomes derived from SUDHL4 cells cultured in normoxia (20%) or hypoxia (1%) for 24 h were used for validation of angiogeneic activity, such as tube formation assay. The exosome secreted from SUDHL4 cells in hypoxic condition significantly enhanced tube formation by HUVECs when compared with exosome obtained from SUDHL4 cell in normoxic condition. To identify cellular and exosomal miRNAs universally responding to hypoxic condition, we assess the expression profiles of intercellular and extracellular miRNAs in SUDHL4 cells cultured in normoxia (20%) or hypoxia (1%) for 24 h using Taqman MicroRNA Array v2.0 (Applied Biosystems, Bedford, MA). SUDHL4 cells were cultured for 24 hours under hypoxic conditions (1% O2) or normoxic conditions (20% O2). The exosome fraction was obtained from culture medium using Exoquick Exosome Precipitation Solution (System Biosciences, Mountain View, CA, USA). Isolation of cellular and exosomal miRNAs was performed using the miRNsasy kit (Qiagen). The expression profile of miRNAs was determined using the Human Taqman miRNA Arrays A (Applied Biosystems). RNU6B and a spike control (ath-miR159) were used as an invariant control for the cell and exosome, respectively. QRT-PCR was carried out on an Applied Biosystems 7900HT thermal cycler using the manufacturerM-bM-^@M-^Ys recommended program. Finally, all the raw data from each array was run on Data Assist Software ver.3.1 (Applied Biosystems).
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Project description:Recently, the existence of extracellular miRNAs enclosed in exosomes has raised the possibility that they play an important role in cell-cell communication. To gain more insight into cell-cell communication via exosomal miRNAs, we investigated whether or not tumor cells exposed to hypoxia secrete exosomes which may affect angiogeneic activity. We used SUDHL4 cells, as donor cells, and HUVECs as recipient cells. Exosomes derived from SUDHL4 cells cultured in normoxia (20%) or hypoxia (1%) for 24 h were used for validation of angiogeneic activity, such as tube formation assay. The exosome secreted from SUDHL4 cells in hypoxic condition significantly enhanced tube formation by HUVECs when compared with exosome obtained from SUDHL4 cell in normoxic condition. To identify cellular and exosomal miRNAs universally responding to hypoxic condition, we assess the expression profiles of intercellular and extracellular miRNAs in SUDHL4 cells cultured in normoxia (20%) or hypoxia (1%) for 24 h using Taqman MicroRNA Array v2.0 (Applied Biosystems, Bedford, MA).
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Project description:Using ChIP-seq, we identified the genome-wide targets of BCL6 and LSD1 in lymphoma cells SUDHL4 and performed H3K4me1 ChIP-seq in cells treated with control siRNA or siRNA targeted to BCL6.
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Project description:Tight regulation of Toll-like receptor (TLR)-mediated inflammatory responses is important in innate immunity. Here, we show that T cell death-associated gene 51 (TDAG51/PHLDA1) is a novel coactivator of the transcription factor FoxO1, regulating inflammatory mediator production in the lipopolysaccharide (LPS)-induced inflammatory response. TDAG51 induction by LPS stimulation was mediated by the TLR2/4 signaling pathway in bone marrow-derived macrophages (BMMs). LPS-induced inflammatory mediator production was significantly decreased in TDAG51-deficient BMMs. In TDAG51-deficient mice, LPS- or pathogenic Escherichia coli infection-induced lethal shock was reduced by decreasing serum proinflammatory cytokine levels. The recruitment of 14-3-3 to FoxO1 was competitively inhibited by the TDAG51-FoxO1 interaction, leading to blockade of FoxO1 cytoplasmic translocation and thereby strengthening FoxO1 nuclear accumulation. TDAG51/FoxO1 double-deficient BMMs showed significantly reduced inflammatory mediator production compared with TDAG51- or FoxO1-deficient BMMs. TDAG51/FoxO1 double deficiency protected mice against LPS- or pathogenic E. coli infection-induced lethal shock by weakening the systemic inflammatory response. Thus, these results indicate that TDAG51 acts as a coactivator of the transcription factor FoxO1, leading to strengthened FoxO1 activity in the LPS-induced inflammatory response.
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Project description:PAX3-FOXO1 is a fusion transcription factor that is the main driver of tumorigenesis leading to the development of alveolar rhabdomyosarcoma (aRMS). Since aRMS cells are addicted to PAX3-FOXO1 activity, the fusion protein also represents a major target for therapeutic interference, which is however challenging as transcription factors usually cannot be inhibited directly by small molecules. Hence, characterization of the biology of PAX3-FOXO1 might lead to the discovery of new possibilities for an indirect inhibition of its activity. Here, our goal was to characterize the proteomic neighborhood of PAX3-FOXO1 and to find candidates potentially affecting its activity and tumor cell viability. Towards this aim, we expressed BirA fused versions of PAX3-FOXO1 (N- and C-terminal) in HEK293T cells under presence of biotin. In the control setup, we expressed the BirA enzyme alone. After Streptavidin purification of biotinylated proteins, we performed mass spectrometry and quantified relative abundances compared to control conditions. This enabled us to determine PAX3-FOXO1 proximal proteins, which we investigated further in orthogonal endogenous systems.
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