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Epithelial deletion of CUL4B increased myeloid-derived suppressor cells-mediated immunosuppression to promote ApcMin/+ tumor formation

GSE189382 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2024/11/20 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 12 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
12 samples
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)
Cullin 4B (CUL4B) is a scaffold protein of E3 ubiquitin ligase complex and has been found frequently overexpressed in various types of cancer. By repressing tumor suppressors, CUL4B is indicated as pro-oncogenic gene in oncogenesis. Reversely, recent studies reveal that deletion of CUL4B in hematopoietic system exerts tumor suppressive effect in tumor bearing hosts.
Read the full summary ↓
However, the role of CUL4B in tumor initiation remains unknown. Here we report that CUL4B deficiency in the intestinal epithelium accelerates ApcMin/+ tumor formation. CUL4B in cancer cells restricts the accumulation of tumor-infiltrating CD11b+Gr-1+ MDSCs to prohibit the adenoma permissive microenvironment and thus increases the number of antitumor CD8+ T cells. Addition of MDSCs to ex vivo cultured ApcMin/+; Cul4bΔIEC tumor organoids rescues their phenotypic alteration in stemness, suggesting a reciprocally strengthened immunosuppressive effect between CUL4B deficient tumor cells and MDSCs. Mechanistically, inhibiting CUL4B epigenetically activates the expression of secreted chemokines and proteins including G-CSF to enroll MDSCs. Our findings suggest that epithelial deletion of CUL4B creates a tumor-prone microenvironment during ApcMin/+ tumor formation and provide a potential strategy to overcome colon cancer initiation and progress in the Wnt-disturbed context.
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 GSE189382_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA782872 and SRA study SRP347409. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 12 more — browse all 12 samples with per-sample file links →

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