GEO series
Multiomic Analyses Reveal New Targets of Polycomb Repressor Complex 2 in Schwann Lineage Cells and Malignant Peripheral Nerve Sheath Tumors - ChIPseq
GSE263109
Homo sapiens (human)
ChIP-seq / ATAC-seq (genome binding and open chromatin)
48 samples
Submitted 2024/04/03
Platform GPL24676
At a glance
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 48 samples
- What it is
- ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
- Organism
- Homo sapiens (human)
- Samples
- 48 samples: 48 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
- Data you can get
- A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Background Malignant peripheral nerve sheath tumors (MPNST) can arise from atypical neurofibromas (ANF). Loss of the polycomb repressor complex 2 (PRC2) is a common event. Previous studies on PRC2-regulated genes in MPNST used genetic addback experiments in highly aneuploid MPNST cell lines which may miss PRC2-regulated genes in NF1-mutant ANF-like precursor cells.
Read the full summary ↓
A set of PRC2-regulated genes in human Schwann cells has not been defined. We hypothesized PRC2 loss has direct and indirect effects on gene expression resulting in MPNST, so we sought PRC2-regulated genes in immortalized human Schwann cells (iHSCs). Methods We engineered NF1-deficient iHSCs with loss of function SUZ12 or EED mutations. RNA sequencing revealed 1,327 differentially expressed genes to define PRC2-regulated genes. To investigate MPNST pathogenesis we compared genes in iHSCs to consistent gene expression differences between ANF and MPNSTs. Chromatin immunoprecipitation sequencing was used to further define targets. Methylome and proteomic analyses were performed to further identify enriched pathways. Results We identified potential PRC2-regulated drivers of MPNST progression. Pathway analysis indicates many upregulated cancer-related pathways. We found transcriptional evidence for activated Notch and Sonic Hedgehog signaling in PRC2-deficient iHSCs. Functional studies confirm Notch signaling is active in MPNST cell lines, patient derived xenografts, and transient cell models of PRC2 deficiency. A combination of MEK and γ-secretase inhibition shows synergy in MPNST cell lines. Conclusions We report PRC2-regulated genes and potential drivers of MPNSTs. Our findings support the Notch pathway as a druggable target in MPNSTs. Our identification of PRC2-regulated genes and pathways could result in more novel therapeutic approaches.
This dataset
Download · which file do I need?
Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.
1 · Just have a look
Processed table
The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.
2 · Re-analyse it
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE263109_RAW.tar (it can run to tens of gigabytes).
3 · Start from the raw reads
Raw sequencing reads
The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.
What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.
Also filed as BioProject PRJNA1096051 and SRA study SRP499624. Searching any of these in the dataset finder brings you back here.
Study design
48 samples, each with a distinct title — no replicated groups
Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.
How we read this: Read from 48 sample titles: 48 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.
Samples in this study
- GSM8185871 eihsc, NF1 proficient; SUZ12 deficient, origin 3.14, ChIP none
- GSM8185872 eihsc, NF1 proficient; SUZ12 deficient, origin 3.14, ChiP H3K27ac
- GSM8185873 eihsc, NF1 proficient; SUZ12 deficient, origin 3.14, ChiP H3K27me3
- GSM8185874 eihsc, NF1 proficient; SUZ12 deficient, origin 3.15, ChiP none
- GSM8185875 eihsc, NF1 proficient; SUZ12 deficient, origin 3.15, ChiP H3K27ac
- GSM8185876 eihsc, NF1 proficient; SUZ12 deficient, origin 3.15, ChiP H3K27me3
- GSM8185877 eihsc, NF1 proficient; SUZ12 deficient, origin 3.7, ChiP none
- GSM8185878 eihsc, NF1 proficient; SUZ12 deficient, origin 3.7, ChiP H3K27ac
- GSM8185879 eihsc, NF1 proficient; SUZ12 deficient, origin 3.7, ChiP H3K27me3
- GSM8185880 eihsc, NF1 deficient; SUZ12 deficient, origin 32.3, ChiP none
- GSM8185881 eihsc, NF1 deficient; SUZ12 deficient, origin 32.3, ChiP H3K27ac
- GSM8185882 eihsc, NF1 deficient; SUZ12 deficient, origin 32.3, ChiP H3K27me3
- GSM8185883 eihsc, NF1 deficient; SUZ12 deficient, origin 32.4, ChiP H3K27ac
- GSM8185884 eihsc, NF1 deficient; SUZ12 deficient, origin 32.4, ChiP H3K27me3
- GSM8185885 eihsc, NF1 deficient; SUZ12 deficient, origin 32.9, ChiP none
- GSM8185886 eihsc, NF1 deficient; SUZ12 deficient, origin 32.9, ChiP H3K27me3
- GSM8185887 eihsc, NF1 deficient; SUZ12 deficient, origin 32.9, ChiP H3K27ac
- GSM8185888 eihsc, NF1 deficient; EED deficient, origin 32.12, ChiP none
- GSM8185889 eihsc, NF1 deficient; EED deficient, origin 32.12, ChiP H3K27me3
- GSM8185890 eihsc, NF1 deficient; EED deficient, origin 32.13, ChiP none
- GSM8185891 eihsc, NF1 deficient; EED deficient, origin 32.13, ChiP H3K27me3
- GSM8185892 eihsc, NF1 deficient, origin 32.1, ChiP none
- GSM8185893 eihsc, NF1 deficient, origin 32.1, ChiP H3K27ac
- GSM8185894 eihsc, NF1 deficient, origin 32.1, ChiP H3K27me3
- GSM8185895 eihsc, NF1 deficient, origin 32.2, ChiP none
- GSM8185896 eihsc, NF1 deficient, origin 32.2, ChiP H3K27ac
- GSM8185897 eihsc, NF1 deficient, origin 32.2, ChiP H3K27me3
- GSM8185898 eihsc, NF1 deficient, origin 32.3, ChiP none
- GSM8185899 eihsc, NF1 deficient, origin 32.3, ChiP H3K27me3
- GSM8185900 eihsc, NF1 deficient, origin 32.3, ChiP H3K27ac
- GSM8185901 eihsc, NF1 deficient; EED deficient, origin 32.12, ChiP H3K27ac
- GSM8185902 eihsc, NF1 deficient; EED deficient, origin 32.13, ChiP H3K27ac
- GSM8185903 eihsc, NF1 proficient; EED deficient, origin 3.8, ChiP none
- GSM8185904 eihsc, NF1 proficient; EED deficient, origin 3.8, ChiP H3K27me3
- GSM8185905 eihsc, NF1 proficient; EED deficient, origin 3.8, ChiP H3K27ac
- GSM8185906 eihsc, NF1 proficient; EED deficient, origin 3.9, ChiP none
- GSM8185907 eihsc, NF1 proficient; EED deficient, origin 3.9, ChiP H3K27me3
- GSM8185908 eihsc, NF1 proficient; EED deficient, origin 3.9, ChiP H3K27ac
- GSM8185909 eihsc, NF1 proficient; SUZ12 proficient, origin 3.1, ChiP none
- GSM8185910 eihsc, NF1 proficient; SUZ12 proficient, origin 3.1, ChiP H3K27ac
+ 8 more — browse all 48 samples with per-sample file links →
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